TumW Cancer Research Results

TumW, Tumor Weight: Click to Expand ⟱

Source:

Type:

Tumor Weight

Scientific Papers found: Click to Expand⟱

3BP,

CET,

3-Bromopyruvate overcomes cetuximab resistance in human colorectal cancer cells by inducing autophagy-dependent ferroptosis

in-vitro,

CRC,

DLD1

NA,

HCT116

eff↑, Our results demonstrated that the co-treatment of 3-BP and cetuximab synergistically induced an antiproliferative effect in both CRC cell lines
Ferroptosis↓, co-treatment induced ferroptosis, autophagy, and apoptosis.
TumAuto↑,
Apoptosis↑,
FOXO3↑, co-treatment inhibited FOXO3a phosphorylation and degradation and activated the FOXO3a/AMPKα/pBeclin1 and FOXO3a/PUMA pathways, leading to the promotion of ferroptosis, autophagy, and apoptosis in DLD-1
AMPKα↑,
p‑Beclin-1↑,
HK2↓, 3-Bromopyruvate (3-BP), also known as hexokinase II inhibitor II, has shown promise as an anticancer agent against various types of cancer
ATP↓, 3-BP exerts its anticancer effects by manipulating cell energy metabolism and regulating oxidative stress, as evidenced by the accumulation of reactive oxygen species (ROS) [13,14,15,16].
ROS↑,
Dose↝, Eight days postinoculation, xenografted mice were randomly divided into four groups and intraperitoneally injected with PBS, 3-BP, cetuximab, or a combination of 3-BP and cetuximab every four days for five injections.
TumVol↓, 3-BP alone or co-treatment with 3-BP and cetuximab significantly reduced the tumor volume and tumor weight on Day 28, but co-treatment showed a greater reduction than 3-BP alone
TumW↓,
xCT/SLC7A11↑, The protein level of SLC7A11 was significantly upregulated in all three cell lines following co-treatment (Fig. 2B).
GSH↓, co-treatment with 3-BP and cetuximab led to glutathione (GSH) depletion (Fig. 2D), reactive oxygen species (ROS) production
eff↓, Knockdown of either ATG5 or Beclin1 attenuated the cell death and MDA production induced by co-treatment
MDA↑,

1069-

AL,

Allicin promotes autophagy and ferroptosis in esophageal squamous cell carcinoma by activating AMPK/mTOR signaling

vitro+vivo,

ESCC,

TE1

10 mg/kg

12.03 μg/mL

mice

vitro+vivo,

ESCC,

KYSE-510

16.76 μg/mL

in-vitro,

Nor,

Het-1A

>160 μg/mL

TumCP↓,
LC3‑Ⅱ/LC3‑Ⅰ↑,
p62↓,
p‑AMPK↑,
mTOR↓,
TumAuto↑,
NCOA4↑,
MDA↑,
Iron↑, elevated malondialdehyde and Fe2+ production levels
TumW↓,
TumVol↓,
ATG5↑,
ATG7↑,
TfR1/CD71↓,
FTH1↓, suppressed the expression of ferritin heavy chain 1 (the major intracellular iron-storage protein)
ROS↑,
Iron↑,
Ferroptosis↑,
*toxicity↓, 80 μg/mL allicin for 24 h did not change the viability of Het-1A cells. A slight reduction in cell viability was observed when Het-1A cells were treated with 160 μg/mL allicin for 24 h

1354-

And,

Andrographolide induces protective autophagy and targeting DJ-1 triggers reactive oxygen species-induced cell death in pancreatic cancer

in-vitro,

PC,

0, 10, 20, 40 µM

in-vivo,

PC,

Apoptosis↑,
DJ-1↓, reduction in DJ-1 expression caused by Andro led to ROS accumulation
ROS↑,
TumAuto↑,
TumCCA↑, G2/M phase
TumCP↓,
TumW↓,
eff↓, pro-apoptotic effect of Andro was attenuated when NAC was co-administered

177-

Api,

Inhibition of MDA-MB-231 breast cancer cell proliferation and tumor growth by apigenin through induction of G2/M arrest and histone H3 acetylation-mediated p21WAF1/CIP1 expression

in-vitro,

BC,

MDA-MB-231

Cyc↓, Cyclin A
CycB/CCNB1↓,
CDK1↓,
P21↑,
PCNA↝,
HDAC↓, apigenin treatment for 48 h suppressed HDAC activity in MDA-MB-231 cells in a dose-dependent manner
TumCP↓, Apigenin Inhibited MDA-MB-231 Cell Proliferation
TumCCA↑, Apigenin Induced G2/M Arrest in MDA-MB-231 Cells
ac‑H3↑, H3 acetylation increased in time-dependent
TumW↓, apigenin treatment significantly reduced the tumor volume and tumor weight
TumVol↓,

2319-

Api,

Apigenin sensitizes radiotherapy of mouse subcutaneous glioma through attenuations of cell stemness and DNA damage repair by inhibiting NF-κB/HIF-1α-mediated glycolysis

in-vitro,

GBM,

 apigenin 20 mg/kg for 12 days

Glycolysis↓, Apigenin inhibited the activities of glycolytic enzymes and expressions of nuclear factor kappa B (NF-κB) p65, hypoxia inducible factor-lα (HIF-1α), glucose transporter (GLUT)-1/3 and pyruvate kinase isozyme type M2 (PKM2) proteins in tumor tissues.
NF-kB↓,
p65↓,
Hif1a↓,
GLUT1↓,
GLUT3↓,
PKM2↓,
RadioS↑, Apigenin sensitizes the radiotherapy of SU3-5R cells-inoculated subcutaneous glioma
TumVol↓, Moreover, the tumor weight and relative tumor weight in the three treatment groups were significantly lower than those in the control group
TumW↓,

1546-

Api,

Apigenin in Cancer Prevention and Therapy: A Systematic Review and Meta-Analysis of Animal Models

Review,

NA,

TumVol↓, Apigenin reduces tumor volume (SMD=-3.597, 95% CI: -4.502 to -2.691, p<0.001)
TumW↓, tumor-weight (SMD=-2.213, 95% CI: -2.897 to -1.529, p<0.001)
AntiCan↑, tumor number (SMD=-1.081, 95% CI: -1.599 to -0.563, p<0.001) and tumor load (SMD=-1.556, 95% CI: -2.336 to -0.776, p<0.001).
Apoptosis↑, exerts anti-tumor effects mainly by inducing apoptosis/cell-cycle arrest
TumCCA↑,

1564-

Api,

Apigenin-induced prostate cancer cell death is initiated by reactive oxygen species and p53 activation

in-vitro,

Pca,

22Rv1

10–80 μM

in-vivo,

NA,

MDM2↓, downregulation of MDM2 protein
NF-kB↓, Exposure of 22Rv1 cells to 20 μM apigenin caused a decrease in NF-κB/p65 transcriptional activity by 24% at 12 h, which was further decreased to 41% at 24 h
p65↓,
P21↑,
ROS↑, Apigenin at these doses resulted in ROS generation
GSH↓, which was accompanied by rapid glutathione depletion
MMP↓, disruption of mitochondrial membrane potential
Cyt‑c↑, cytosolic release of cytochrome c
Apoptosis↑,
P53↑, accumulation of a p53 fraction to the mitochondria, which was rapid and occurred between 1 and 3 h after apigenin treatment
eff↓, All these effects were significantly blocked by pretreatment of cells with the antioxidant N-acetylcysteine
Bcl-xL↓,
Bcl-2↓,
BAX↑,
Casp↑, triggering caspase activation
TumCG↓, in vivo mice
TumVol↓, tumor volume was inhibited by 44 and 59%
TumW↓, wet weight of tumor was decreased by 41 and 53%

1563-

Api,

MET,

Metformin-induced ROS upregulation as amplified by apigenin causes profound anticancer activity while sparing normal cells

in-vitro,

Nor,

HDFa

metformin (5 mM), apigenin (1 or 20 µM),

in-vitro,

PC,

AsPC-1

in-vitro,

PC,

MIA PaCa-2

in-vitro,

Pca,

DU145

in-vitro,

Pca,

LNCaP

in-vivo,

NA,

mice

selectivity↑, Metformin increased cellular ROS levels in AsPC-1 pancreatic cancer cells, with minimal effect in HDF, human primary dermal fibroblasts.
selectivity↑, Metformin reduced cellular ATP levels in HDF, but not in AsPC-1 cells
selectivity↓, Metformin increased AMPK, p-AMPK (Thr172), FOXO3a, p-FOXO3a (Ser413), and MnSOD levels in HDF, but not in AsPC-1 cells
ROS↑,
eff↑, Metformin combined with apigenin increased ROS levels dramatically and decreased cell viability in various cancer cells including AsPC-1 cells, with each drug used singly having a minimal effect.
tumCV↓,
MMP↓, Metformin/apigenin combination synergistically decreased mitochondrial membrane potential in AsPC-1 cells but to a lesser extent in HDF cells
Dose∅, co-treatment with metformin (0.05, 0.5 or 5 mM) and apigenin (20 µM) dramatically increased cellular ROS levels in AsPC-1 cells
eff↓, NAC blocked the metformin/apigenin co-treatment-induced cell death in AsPC-1 cells
DNAdam↑, Combination of metformin and apigenin leads to DNA damage-induced apoptosis, autophagy and necroptosis in AsPC-1 cells but not in HDF cells
Apoptosis↑,
TumAuto↑,
Necroptosis↑,
p‑P53↑, p-p53, Bim, Bid, Bax, cleaved PARP, caspase 3, caspase 8, and caspase 9 were also significantly increased by combination of metformin and apigenin in AsPC-1
BIM↑,
BAX↑,
p‑PARP↑,
Casp3↑,
Casp8↑,
Casp9↑,
Cyt‑c↑, Cytochrome C was also released from mitochondria in AsPC-1 cell
Bcl-2↓,
AIF↑, Interestingly, autophagy-related proteins (AIF, P62 and LC3B) and necroptosis-related proteins (MLKL, p-MLKL, RIP3 and p-RIP3) were also increased by combination of metformin and apigenin
p62↑,
LC3B↑,
MLKL↑,
p‑MLKL↓,
RIP3↑,
p‑RIP3↑,
TumCG↑, in vivo
TumW↓, metformin (125 mg/kg) or apigenin (40 mg/kg) caused a reduction of tumor size compared to the control group (Fig. 7D). However, oral administration of combination of metformin and apigenin decreased tumor weight profoundly

1028-

ASA,

Aspirin Suppressed PD-L1 Expression through Suppressing KAT5 and Subsequently Inhibited PD-1 and PD-L1 Signaling to Attenuate OC Development

vitro+vivo,

Ovarian,

TumCP↓,
TumW↓,
PD-L1↓,
Ki-67↓,
H3K27ac∅, ASP downregulated KAT5 expression and blocked this phenomenon.
eff↑, effect of antiPD-L1 therapy

1179-

Ash,

Withaferin-A Inhibits Colon Cancer Cell Growth by Blocking STAT3 Transcriptional Activity

in-vitro,

CRC,

HCT116

in-vivo,

NA,

mouse

TumCP↓,
TumCMig↓,
STAT3↓, implicated in the development and progression of colon cancer.
TumVol↓,
TumW↓,

2001-

Ash,

Withania somnifera: from prevention to treatment of cancer

Review,

Var,

toxicity↓, Some sedation, ptosis and ataxia were observed in Sprague-Dawley rats 15–20 minutes of administering a herbal concoction that contained WS at a large dose of 1–2 g/kg body weight [36]
TumW↓, Induction of apoptosis by WA has been noted in some in vivo models where treatment with 4 mg/kg WA, i.p. 5 times for 2 weeks markedly reduced MDA-MB-231 tumor weights in nude mice as well as increased apoptosis compared to tumors in control mice [56
Dose?, 20 mg/kg, oral 3X/wk for 14 wk Hamster Head and Neck Example
eff↝, showed that this chemopreventive capacity was dependent on a circadian pattern where hamsters dosed with WA at 8 AM and 12 PM showed 100% protection from oral tumor formation while those treated at 12 AM showed 50% incidence in oral tumors
Ki-67↓, WA treatment resulted in retarded tumor growth; reduction in cell proliferation marker Ki-67, survivin, and XIAP,
survivin↓,
XIAP↓,
PERK↑, higher protein expression of pERK, pRSK, CHOP and DR-5 was also observed in the WA-treated group compared to control.
p‑RSK↑,
CHOP/DDIT3↑,
DR5↑,
Dose↝, Clinically diagnosed schizophrenia patients who had received antipsychotic medications for 6 months or more received either a capsule with 400 mg of WS extract (n=15), three times daily, for 1 month [80]
BG↓, Results after one month showed significant reduction in serum triglycerides and fasting blood glucose levels in the WS extract- treated group compared to the placebo
DNMTs↓, in MCF7 and MDA-MB-231 breast cancer cells WA treatment suppressed transcription of DNMT.

2599-

Ba,

Baicalein induces apoptosis and autophagy of breast cancer cells via inhibiting PI3K/AKT pathway in vivo and vitro

in-vitro,

BC,

MCF7

0, 10, 20, and 40 µM

14uM

 IC50 values of baicalein at 24, 48, and 72 hours were 51.06, 22.16, and 13.98 µM

in-vitro,

BC,

MDA-MB-231

60.12, 27.98, and 19.01 µM

in-vivo,

NA,

Female BALB/c nude mice

TumCP↓, baicalein has the potential to suppress cell proliferation, induce apoptosis and autophagy of breast cancer cells in vitro and in vivo.
Apoptosis↑,
p‑Akt↓, baicalein significantly downregulated the expression of p-AKT, p-mTOR, NF-κB, and p-IκB
p‑mTOR↓,
NF-kB↓,
p‑IKKα↓,
IKKα↑, while enhancing the expression of IκB in MCF-7 and MDA-MB-231
PI3K↓, baicalein induces apoptosis and autophagy of breast cancer cells via inhibiting the PI3K/AKT signaling pathway in vivo and vitro
MMP↓, increasing dose of baicalein, the ΔΨm was decreased in MCF-7 and MDA-MB-231 cells.
TumAuto↑, Baicalein induces autophagy in MCF-7 and MDA-MB-231 cells
TumVol↓, demonstrated that the growth, volume, and weight of tumors were significantly suppressed in the baicalein-treated group compared with the control group
TumW↓,

5658-

BNL,

Natural borneol is a novel chemosensitizer that enhances temozolomide-induced anticancer efficiency against human glioma by triggering mitochondrial dysfunction and reactive oxide species-mediated oxidative damage

vitro+vivo,

GBM,

U251

 nude mice

ChemoSen↑, combined treatment of NB and TMZ more effectively inhibited human glioma growth via triggering mitochondria-mediated apoptosis in vitro, accompanied by the caspase activation.
mt-Apoptosis↑,
Casp↑,
DNAdam↑, NB enhanced TMZ-induced DNA damage through inducing reactive oxide species (ROS) overproduction.
ROS↑,
angioG↓, anti-angiogenesis.
BBB↑, It is reported that NB could improve the oral bioavailability of anti-tumor drugs by regulating the permeability of the BBB.
EPR↑,
TumVol↓, combined treatment of NB and TMZ significantly inhibited tumor volume and tumor weight compared to that in treatment with NB or TMZ alone
TumW↓,
BioEnh↑,

5880-

CAR,

In vitro and in vivo antitumor potential of carvacrol nanoemulsion against human lung adenocarcinoma A549 cells via mitochondrial mediated apoptosis

vitro+vivo,

Lung,

A549

nude mice, present study commenced to formulate CANE by an energy intensive ultrasonication method.

in-vitro,

Nor,

BEAS-2B

in-vitro,

Lung,

PC9

Dose↝, prepare a carvacrol nanoemulsion (CANE) using an ultrasonication technique and further evaluation of its anticancer potential against human lung adenocarcinoma A549 cells. (160nm)
mt-ROS↑, The CANE induced reactive oxygen species (ROS) production in A549 cells,
p‑JNK↑, leading to activation of key regulators of apoptosis such as p-JNK, Bax and Bcl2 as well as release of cytochrome C, and activation of the caspase cascade.
BAX↑,
Cyt‑c↑,
Casp↑,
AntiTum↑, CANE displayed a strong antitumor potential in vivo using an athymic nude mice model.
ER Stress↑, Abnormally high ROS levels create ER stress with the involvement of three major signaling proteins IRE1-α, PERK and ATF-6
LDH↑, higher LDH activity, which is a well-established biomarker released by damaged cells, was observed in CANE-treated cells
selectivity↑, CANE displayed no cytotoxicity up to 100 µg/ml against normal bronchial epithelium cells (BEAS-2B)
Apoptosis↑, Induction of apoptosis and ROS production in the presence of CANE
DNAdam↑, potential role on DNA damage and chromatin condensation
IRE1↑, We observed a higher expression of IRE1-α in CANE treated cells
XBP-1↑, similar expression pattern for XBP-1
CHOP/DDIT3↓, down-regulation of CHOP, p-eIF2α, and GRP78 was observed in CANE-treated cells
p‑eIF2α↓,
GRP78/BiP↓,
Ca+2↑, increase of Ca+2 levels in CANE-treated cells. A 2.5 fold higher Ca+2 was observed at 100 μg/ml CANE treated cells
MMP↓, CANE severely altered mitochondrial membrane potential (Δψm) in a dose-dependent manner.
Bcl-2↓, up- and down-regulation of pro-apoptotic (Bax) and anti-apoptotic (Bcl2) proteins
Casp3↑, higher levels of cleaved caspase-9 and caspase-3 in cells treated with CANE in a dose-dependent manner
Casp9↑,
eff↓, To confirm this, A549 cells were first treated with N-acetyl-L-cysteine NAC (5 mM), a strong scavenger of ROS, prior to CANE (100 µg/ml) treatment and observed a marked reduction in ROS generation
TumW↓, A significant (p < 0.05) 34.2 and 62.1% reduction in tumor weight was observed in the mice treated with 50 and 100 mg/Kg CANE, orally three times in a week
Weight↑, body weights of 100 mg/kg CANE treated mice remained static up to the second week and increased further up to 4 weeks
eff↑, ultrasonication consider as simple, cost-effective, clean and prompt aseptic technique16, wherein large droplets ruptured into small droplets by ultrasound leading to the formation of nano-scale droplets
eff↑, We selected polysorbate 80 as a surfactant (HLB, 15), which is regarded as safe for using in pharmaceutical and food industries1

1103-

CBD,

Cannabidiol inhibits invasion and metastasis in colorectal cancer cells by reversing epithelial-mesenchymal transition through the Wnt/β-catenin signaling pathway

vitro+vivo,

NA,

Apoptosis↑,
TumCP↓,
TumCMig↓,
TumMeta↓,
EMT↓,
E-cadherin↑,
N-cadherin↓,
Snail↓,
Vim↓,
Hif1a↓,
Wnt/(β-catenin)↓,
AXIN1↑,
TumVol↓, orthotopic xenograft tumors
TumW↓,

5940-

Cela,

Celastrol Suppresses Angiogenesis-Mediated Tumor Growth through Inhibition of AKT/Mammalian Target of Rapamycin Pathway

in-vivo,

Pca,

PC3

mice

Dose↝, When administered subcutaneously to mice bearing human prostate cancer (PC-3 cell) xenografts, Celastrol (2 mg/kg/d)
TumVol↓, significantly reduced the volume and the weight of solid tumors and decreased tumor angiogenesis.
TumW↓,
angioG↓,
VEGF↓, this agent inhibited vascular endothelial growth factor (VEGF)-induced proliferation, migration, invasion,
TumCMig↓,
TumCP↓,
TumCI↓,
Akt↓, Celastrol suppressed the VEGF-induced activation of AKT, mammalian target of rapamycin (mTOR), and ribosomal protein S6 kinase (P70S6K)
mTOR↓,
P70S6K↓,

6654-

CGA,

Chlorogenic acid induces 4T1 breast cancer tumor's apoptosis via p53, Bax, Bcl-2, and caspase-3 signaling pathways in BALB/c mice

in-vivo,

BC,

4T1

BALB/c mice

TumW↓, CGA reduced tumor weight and volume in the PR group (P < .05) and in the TM group (P < .001). Surprisingly, it eliminated the tumors in the TM group.
TumVol↓,
TumMeta↓, Metastatic nodules in the PR and TM groups were significantly reduced as compared with the BC group (P < .001).
Bax:Bcl2↑, CGA therapy increased the expression ratio of Bax/Bcl-2 (P < .001 and P < .05, respectively) and the expression of p53
P53↑,
Casp3↑, and caspase-3 genes (P < .01) in the PR and TM groups.

1106-

CGA,

Chlorogenic Acid Inhibits Epithelial-Mesenchymal Transition and Invasion of Breast Cancer by Down-Regulating LRP6

vitro+vivo,

BC,

MCF7

E-cadherin↑,
ZO-1↑,
Zeb1↓,
N-cadherin↓,
Vim↓,
Snail↓,
Slug↓,
MMP2↓,
MMP9↓,
TumCMig↓,
TumCI↓,
LRP6↓,
p‑LRP6↓,
β-catenin/ZEB1↓,
TumVol↓, in vivo
TumW↓,

7159-

CHA,

ROS-mediated inactivation of the PI3K/AKT pathway is involved in the antigastric cancer effects of thioredoxin reductase-1 inhibitor chaetocin

vitro+vivo,

GC,

HGC27

in-vitro,

GC,

AGS

in-vitro,

GC,

BGC-823

in-vitro,

GC,

SGC-7901

in-vitro,

Nor,

HEK293

TumCP↓, In this study, we showed that chaetocin, a natural product isolated from the Chaetomium species of fungi, inhibited proliferation, induced G 2/M phase arrest and caspase-dependent apoptosis in both in vitro and in vivo models
TumCCA↑,
Casp↑,
Apoptosis↑,
TrxR1↓, Chaetocin inactivated TRXR-1, resulting in the accumulation of reactive oxygen species (ROS) in GC cells;
ROS↑, results suggest that chaetocin induces ROS production by inhibiting the TRX-TRXR system and that this ROS production is required for chaetocin-mediated apoptosis in GC cells.
eff↓, cotreatment of GC cells with the ROS scavenger N-acetyl-L-cysteine (NAC) attenuated chaetocin-induced apoptosis
eff↑, chaetocin-induced apoptosis was significantly increased when GC cells were cotreated with auranofin.
PI3K↓, chaetocin was shown to inactivate the PI3K/AKT pathway by inducing ROS generation;
Akt↓,
TumCG↓, Chaetocin inhibits the growth of GC cells
cl‑PARP↑, chaetocin-induced PARP cleavage (an indicator of apoptosis) in HGC-27 and AGS cells.
cl‑Casp3↑, increased the cleaved forms of caspase-3, −9, and −8 in HGC-27 and AGS cells, illustrating that chaetocin may induce caspase-dependent apoptosis of GC cells
cl‑Casp9↑,
cl‑Casp8↑,
Bcl-2↓, antiapoptotic proteins BCL-2, BCL-XL, MCL-1, XIAP and survivin decreased following chaetocin treatment
Bcl-xL↓,
Mcl-1↓,
XIAP↓,
survivin↓,
TumVol↓, chaetocin effectively reduced the volume and weight of HGC-27 xenograft tumors
TumW↓,
Weight∅, and no significant losses were detected in the body weights of the experimental animals
toxicity↓, chaetocin significantly restrains the growth of GC cell xenografts but has no major side effects in mice
Ki-67↓, ki-67, a biomarker related to proliferation, was downregulated in response to chaetocin
other↝, However, the TRX-TRXR system has recently been found to be upregulated in a variety of human cancers including gastric, colorectal, lung and liver cancers, and overexpression of specific components of this system is linked to tumor cell prof

5985-

Chit,

immuno,

Immunomodulatory potential of chitosan-based materials for cancer therapy: a systematic review of in vitro, in vivo and clinical studies.

Review,

Var,

TumCP↓, Generally, Ch-based formulations increase the recruitment and proliferation of cells associated with pro-inflammatory abilities and decrease cells which exert anti-inflammatory activities.
TumW↓, These effects correlated with a decreased tumor weight, reduced metastases, reversion of the immunosuppressive TME and increased survival in vivo.
OS↑,
eff↑, Overall, Ch-based formulations present the potential for immunotherapy in cancer.

6129-

CHr,

A Chrysin Derivative Suppresses Skin Cancer Growth by Inhibiting Cyclin-dependent Kinases

vitro+vivo,

Melanoma,

 Xenograft Mouse Model

ATP↓, Modified chrysin is a novel ATP-noncompetitive inhibitor.
TumCCA↑, Compound 69407 inhibits G1 to S phase transition and Rb phosphorylation levels in EGF-stimulated JB6 P+ cells
CDK2↓, Compound 69407 inhibits Cdk2 and Cdk4 kinase activities in vitro
CDK4↓,
TumW↓, Compound 69407 was injected into the right flank of individual athymic nude mice. The results showed that the mean tumor weight was decreased in the compound 69407-treated group

952-

Cin,

Cinnamon Extract Reduces VEGF Expression Via Suppressing HIF-1α Gene Expression and Inhibits Tumor Growth in Mice

in-vitro,

BC,

MDA-MB-231

0-30um/ml

mice

in-vitro,

GBM,

U251

in-vivo,

Ovarian,

SKOV3

inoculated in mice

VEGF↓, Cinnamaldehyde, a major component in cinnamon, was identified as one active component in CE that inhibits VEGF expression.
Hif1a↓, inhibit expression and phosphorylation of STAT3 and AKT, which are key factors in the regulation of HIF-1α expression
p‑STAT3↓,
p‑Akt↓,
angioG↓,
TumCG↓,
TumW↓,
ascitic↓, reduction in tumor burden and ascites volume

141-

CUR,

Effect of curcumin on Bcl-2 and Bax expression in nude mice prostate cancer

in-vivo,

Pca,

PC3

 100 mg/kg, 50 mg/kg, and 25 mg/kg curcumin)

 nude mice

BAX↑, Curcumin could inhibit PC-3 growth, decrease tumor volume, reduce tumor weight, and induce cell apoptosis under the skin of nude mice by up-regulating Bax and down-regulating Bcl-2.
Bcl-2↓,
TumCG↓,
TumVol↓,
TumW↓,
Apoptosis↑,
AR↓, Curcumin can down-regulate androgen receptor transcription and expression.
Ca+2↑, Curcumin may control Bax and Bcl-2 expression to induce Ca2+ overload in the mitochondria, resulting mitochondrial permeability transition channels open,
MPT↑,

7445-

CYN,

Cynaropicrin Shows Antitumor Progression Potential in Colorectal Cancer Through Mediation of the LIFR/STATs Axis

vitro+vivo,

CRC,

RKO

 xenograft model.

in-vitro,

CRC,

HCT116

in-vitro,

CRC,

DLD1

tumCV↓, Cynaropicrin significantly reduced the survival ability of human CRC cells and promoted apoptosis in a dose-dependent manner.
STAT↓, mediated by inhibition of the LIFR/STATs axis
LIFR/CD118↓,
STAT3↓, Cynaropicrin reduced the formation of STAT3/STAT4 heterodimers and blocked their entry into the nucleus
STAT4↑,
TumCG?, Cynaropicrin also suppressed tumor growth in the xenograft model.
cl‑PARP1↑, changes in the expression levels of Cl-PARP1, Bcl-2, Bax, which are associated with the process of apoptosis
Bcl-2↓,
BAX↑,
STAT3↓, Cynaropicrin Blocked the Activation of STAT3 via Inhibiting LIFR Activity
Dose↝, intraperitoneal administration of cynaropicrin at doses of 2.5 and 5 mg/kg resulted in decreased tumor volume and weight compared to the vehicle group
TumVol↓,
TumW↓,
toxicity↓, potent antitumor activity against the growth of implanted CRC with minimal toxicity in the animal.

6683-

DCA,

Dichloroacetate for Cancer Treatment: Some Facts and Many Doubts

Review,

Var,

PDK1↓, classic DCA target, pyruvate dehydrogenase kinase
lactateProd↓, reduce lactic acid production which would push the cell towards oxidative phosphorylation: this would be the supposed function of dichloroacetate (DCA).
Apoptosis↑, They found that DCA induced apoptosis and decreased proliferation by restoring mitochondrial oxidative metabolism, without toxicity to normal cells.
TumCP↓,
selectivity↑,
other↝, many clinics, usually called “DCA Clinics” have opened, mainly in Canada and Germany.
Dose↝, DCA is sold over the counter and is produced by many laboratories. The quality of the product from these laboratories is not well established. These particulars explain many of the doubts about DCA’s real value as a therapeutic tool.
BioAv↑, DCA is an orally available molecule that is quickly and almost completely absorbed by the digestive system
Half-Life↓, With a 10 mg/kg infusion the maximum plasma concentration achieved was between 19.9 μg/ml and 24.7 μg/ml with a half life of only 20 minutes. If the infused dose was increased to 20 mg/kg the plasma concentration was between 57.3 and 74.9 μg/ml with
Glycolysis↓, facilitates the switch from a glycolytic to an oxidative metabolism.
OXPHOS↑,
Casp↑, onversion to an oxidative metabolism by DCA, is an increase in caspase-mediated apoptosis
i-pH↓, pHi decreases (at least temporarily).
COX2/PTGS2↑, DCA increases the expression of COX2 and the latter increases tumor resistance to DCA. Therefore, a possible integrated treatment could be COX2 inhibitor co-administered with DCA
Hif1a↓, DCA suppresses HIF-1α activity and angiogenesis through the inhibition of PDK-II
angioG↓,
HMG-CoA↓, figure 7
GSTZ1↓,
OCR↑,
lipoGen↓,
fatigue↓,
survivin↓, Survivin (an inhibitor of apoptosis) expression was decreased and miR-375 (a microRNA which acts as a tumor suppressor) levels were increased.
miR-375↑,
eff↓, African Americans are known to respond poorly to therapy compared with Caucasian American patients.
CSCs↓, DCA can inhibit the cancer stem cell like characteristics of the cells and strongly influenced the metabolic pathway of the cells causing a shift from glycolysis to oxidative phosphorylation.
TumAuto↑, DCA induced autophagy in human colon cancer cells with ROS production and mTOR inhibition,
mTOR↓,
TumCI↓, DCA induced apoptosis, inhibited invasion, and angiogenesis. In mouse experiments in vivo with the melanoma allografts, DCA reduced volume and weight of tumors.
TumVol↓,
TumW↓,
ATP↓, DCA alone reduced glycolytic activity and intracellular ATP levels and inhibited cellular growth in melanoma cells.
Warburg↓, DCA was also found to interrupt the Warburg effect and decreased proliferation.
eff↑, The co-application of metformin and DCA suppressed human liver cancer cell proliferation inducing apoptosis through inhibition of mTORC1 and increased ROS in vitro and in vivo
e-pH↑, when measuring extracellular pH in vivo found that an initial increase in extracellular pH of tumors in mice when treated with DCA.
eff↑, To avoid the development of this type of metabolic resistance DCA should be given simultaneously with other metabolic drugs such as metformin [327] or 2 deoxyglucose.
eff↑, chronic co-administration of DCA with sodium bicarbonate to tumor bearing mice prolonged survival
other↝, High doses of thiamin (vit B1) have effects similar to those of DCA: reduced PDH phosphorylation, reduced lactate prod and increased casp3 activity with reduced proliferation in colon cancer cells. can vitB1 replace DCA as a nontoxic PDK inhibitor?
RadioS↑, Dong et al. [380] found that DCA radiosensitized esophageal carcinoma cells in vitro and in vivo through increased ROS accumulation.
toxicity↓, 25 mg/Kg/day may show a mild sedative effect or drowsiness. The most serious published side effect is reversible peripheral neuropathy
Dose↝, 10 to 50 mg/kg body weight/day has been found to be a safe dose. However, single nucleotide polymorphisms (SNPs) in the gene of the enzyme GSTZ1 cause difficulties in establishing a universal dose [409] as noted above.
eff↑, There is strong evidence showing that the association of metformin and DCA has significant cytotoxic effects.
eff↑, To this approach we must add a third compound: a COX2 inhibitor like celecoxib to decrease COX2 expression induced by DCA.
eff↑, the triple association of DCA, metformin and celecoxib, which has never been experimentally tested in patients, deserves well planned phase II clinical trials.
toxicity↝, DCA will never become a stand-alone chemotherapeutic compound. The fundamental reason for this statement is that the drug can only reach micromolar blood concentrations without toxicity and requires millimolar levels to be cytotoxic.
eff↓, DCA should not be used in association with allopurinol, NSAIDs, or flavonoids because they reduce cellular DCA uptake.

1866-

DCA,

MET,

BTZ,

Targeting metabolic pathways alleviates bortezomib-induced neuropathic pain without compromising anticancer efficacy in a sex-specific manner

in-vivo,

NA,

mice

eff↑, Metformin, DCA, and oxamate effectively attenuated bortezomib-induced neuropathic pain without compromising the anticancer efficacy of bortezomib in both male and female mice.
TumCG↓,
Hif1a↓, Metformin, a widely used antidiabetic drug, has been shown to inhibit the expression of HIF1A
PDH↑, Dichloroacetate (DCA), a small molecule inhibitor, targets PDHK, thereby activating PDH and promoting the entry of pyruvate into the mitochondrial Krebs cycle
lactateProd↓, Oxamate, an analog of pyruvate, inhibits lactate dehydrogenase, thereby reducing the production of lactate and attenuating the pain-inducing effects of extracellular acidification (25) in mice with bortezomib-induced neuropathic pain (4
TumVol↓,
TumW↓,
Glycolysis↑, These findings suggest that targeting aerobic glycolysis with DCA or oxamate can complement the anticancer efficacy of bortezomib in male tumor-bearing mice.
neuroP↑, Metformin and aerobic glycolysis inhibitors attenuate bortezomib-induced neuropathic pain without compromising anticancer efficacy in female tumor-bearing mice

6692-

DFC,

Diclofenac Inhibits Tumor Growth in a Murine Model of Pancreatic Cancer by Modulation of VEGF Levels and Arginase Activity

in-vivo,

PC,

Panc02

mice

TumW↓, We found that diclofenac treatment (30 mg/kg/bw for 11 days) of mice inoculated with PANC02 cells, reduced the tumor weight by 60%, correlating with increased apoptosis of tumor cells.
Apoptosis↑,
VEGF↓, diclofenac drastically decreased tumor vascularization by downregulating VEGF in the tumor and in abdominal cavity fluid.
COX2/PTGS2↓, in contrast to other COX-2 inhibitors, diclofenac increased arginase activity/arginase 1 protein content in tumor stroma cells, peritoneal macrophages and white blood cells by 2.4, 4.8 and 2 fold, respectively.
ARG1/2↑, Diclofenac increases arginase activity in pancreatic tumors and in peritoneal macrophages, but not in bone marrow-CD 115 positive and CD 115 negative cells
TumCG↓, Diclofenac inhibits tumor growth in an orthotopic model of pancreatic cancer in mice
angioG↓, Tumors from diclofenac treated animals were very pale (Fig 1A), suggesting that the treatment caused an antiangiogenic effect.
ARG↓, subsequent arginine depletion and decrease in NO levels, both in serum and peritoneal cavity, adds to tumor growth inhibition by malnourishment and poor vasculature development.
NO↓,

6750-

DHA,

Chemo,

Docosahexaenoic acid (DHA) supplementation attenuates changes in the concentration, phenotype, and response of immune peripheral blood cells in breast cancer patients undergoing neoadjuvant therapy. Secondary findings from the DHA-WIN trial

Trial,

BC,

4.4 g/day of DHA or a placebo for 18 weeks

in conjunction with their neoadjuvant chemotherapy for breast cancer.

*CD14↑, In the placebo group the proportion of T cells (CD3 +), and functionally active monocytes (CD14 + HLA-DR +) was reduced at the last cycle of chemotherapy (15 weeks) but remained constant in the DHA group
*NLR↓, The neutrophil-to-lymphocyte ratio (NLR) was maintained in the DHA group but increased in the placebo at the end of chemotherapy
eff↑, An increase in this ratio was associated with lower chance of achieving pathological complete response
*IL4↑, After 15 weeks of therapy, the DHA-supplemented group had higher concentrations of stimulated cytokines IL-4, IL-10, and the T helper type 1 cytokine IFN-γ after phytohemagglutinin (PHA) challenge, and higher concentrations of TNF-α and IFN-γ cytokin
*IL10↑,
*IFN-γ↑,
*TNF-α↑,
Imm↑, Supplementing DHA during breast cancer neoadjuvant chemotherapy improved systemic immune function by attenuating changes in blood cell concentrations, preventing depletion of immune cells
eff↑, Newell et al. [19] previously demonstrated an improvement in chemotherapy success, measured as reduced tumor weight and Ki67 activity (proliferation) in animals fed DHA (3.9% w/w of total fat) in combination with chemotherapy (docetaxel) i
TumW↓,

6788-

EGCG,

A systematic review and meta-analysis of the effects of green tea extracts and polyphenols in female hormone-dependent cancers for benefit-risk evaluation

Review,

BC,

epigallocatechin gallate (EGCG) on tumor growth indices in mouse and rat models of breast, ovarian, and uterine cancers.

Review,

Ovarian,

TumVol↓, Pooled analysis showed significant reductions in tumor volume (Hedge’s g = -2.332, 95% CI = -3.067 to -1.596, p = 0.000) and tumor weight
TumW↓,
*toxicity↝, No consistent adverse effects were reported in the included studies, though liver function parameters were not assessed.

1056-

EGCG,

EGCG, a major green tea catechin suppresses breast tumor angiogenesis and growth via inhibiting the activation of HIF-1α and NFκB, and VEGF expression

vitro+vivo,

BC,

E0771

50–100 mg/kg/d in drinking water for 4 weeks

mice

TumW↓,
VEGF↓,
Weight∅, no effects on the body weight, heart weight, angiogenesis and VEGF expression in the heart and skeletal muscle of mice.
Hif1a↓,
NF-kB↓,

2309-

EGCG,

Chemo,

Targeting Glycolysis with Epigallocatechin-3-Gallate Enhances the Efficacy of Chemotherapeutics in Pancreatic Cancer Cells and Xenografts

in-vitro,

PC,

MIA PaCa-2

(20–100 μM) for 72 h

in-vitro,

Nor,

HPNE

in-vitro,

PC,

PANC1

in-vivo,

NA,

mice

TumCG↓, EGCG reduced pancreatic cancer cell growth in a concentration-dependent manner
eff↑, and the growth inhibition effect was further enhanced under glucose deprivation conditions.
ROS↑, EGCG at 40 µM increased ROS levels by 1.4- and 1.6-fold in Panc-1 and MIA PaCa-2 cells, respectively
ECAR↓, EGCG affected glycolysis by suppressing the extracellular acidification rate through the reduction of the activity and levels of the glycolytic enzymes phosphofructokinase and pyruvate kinase.
ChemoSen↑, EGCG sensitized gemcitabine to inhibit pancreatic cancer cell growth in vitro and in vivo.
selectivity↑, EGCG at 80 µM for 72 h had significantly less effect on the HPNE cells, reducing cell growth by only 24%
Glycolysis↓, EGCG Inhibits Glycolysis through Suppressing Rate-Limiting Enzymes. EGCG Plus Gemcitabine Further Inhibits Glycolysis
PFK↓, EGCG treatment reduced both the activity and expression levels of phosphofructokinase (PFK) and pyruvate kinase (PK) in Panc-1 and MIA PaCa-2 cells
PKA↓,
HK2∅, EGCG failed to reduce hexokinases II (HK2) and lactate dehydrogenase A (LDHA) protein expression levels
LDHA∅,
PFKP↓, EGCG reduced the levels of PFKP and PKM2 (p < 0.01 for both) in pancreatic tumor xenograft homogenates, obtained from mice treated with EGCG
PKM2↓,
H2O2↑, EGCG at 40 µM increased H2O2 levels by 1.5- and 1.9-fold in Panc-1 and MIA PaCa-2 cells
TumW↓, EGCG and gemcitabine, given as single agents, reduced tumor weight by 40% and 52%, respectively, compared to vehicle-treated controls (p < 0.05 and p < 0.01). In combination, EGCG plus gemcitabine reduced tumor weight by 67%,

6843-

EVO,

Effects of evodiamine on PI3K/Akt and MAPK/ERK signaling pathways in pancreatic cancer cells

in-vivo,

PC,

PANC1

EVO (1.0, 5.0 and 10 µM) for 48 h a

Tumor-bearing nude mice

in-vitro,

PC,

SW1990

Apoptosis↑, Apoptosis increased with increasing EVO concentration.
LC3II↓, EVO decreased LC3II, enhanced P62 and inhibited the expression of Akt, extracellular-signal-regulated protein kinase (ERK)1/2 and p38.
p62↑,
Akt↓,
ERK↓,
p38↓,
TumW↓, tumor weight decreased more markedly in the EVO-treated group.
TumCG↓, EVO markedly inhibited the growth of PC cells.
TumCMig↓, EVO decreases PC cell migration

1112-

FA,

Ferulic acid exerts antitumor activity and inhibits metastasis in breast cancer cells by regulating epithelial to mesenchymal transition

in-vitro,

BC,

MDA-MB-231

in-vivo,

BC,

mouse

tumCV↓,
Apoptosis↑,
AntiTum↑,
TumMeta↓,
EMT↓,
TumVol↓,
TumW↓,

1654-

FA,

Molecular mechanism of ferulic acid and its derivatives in tumor progression

Review,

Var,

AntiCan↑, FA has anti-inflammatory, analgesic, anti-radiation, and immune-enhancing effects and also shows anticancer activity,
Inflam↓,
RadioS↑,
ROS↑, FA can cause mitochondrial apoptosis by inducing the generation of intracellular reactive oxygen species (ROS)
Apoptosis↑,
TumCCA↑, G0/G1 phase
TumCMig↑, inducing autophagy; inhibiting cell migration, invasion, and angiogenesis
TumCI↓,
angioG↓,
ChemoSen↑, synergistically improving the efficacy of chemotherapy drugs and reducing adverse reactions.
ChemoSideEff↓,
P53↑, FA could increase the expression level of p53 in MIA PaCa-2 pancreatic cancer cells
cycD1/CCND1↓, while reducing the expression levels of cyclin D1 and cyclin-dependent kinase (CDK) 4/6.
CDK4↓,
CDK6↓,
TumW↓, FA treatment was found to reduce tumor weight in a dose-dependent manner, increase miR-34a expression, downregulate Bcl-2 protein expression, and upregulate caspase-3 protein expression
miR-34a↑,
Bcl-2↓,
Casp3↑,
BAX↑,
β-catenin/ZEB1↓, isoferulic acid dose-dependently downregulated the expression of β-catenin and MYC proto-oncogene (c-Myc), inducing apoptosis
cMyc↓,
Bax:Bcl2↑, FXS-3 can inhibit the activity of A549 cells by upregulating the Bax/Bcl-2 ratio
SOD↓, After treatment with FA, Cao et al. [40] observed an increase in ROS production and a decrease in superoxide dismutase activity and glutathione content in EC-1 and TE-4 oesophageal cancer cells
GSH↓,
LDH↓, FA could promote the release of lactate dehydrogenase (LDH)
ERK↑, A can activate the ERK1/2 pathway
eff↑, conjugated zinc oxide nanoparticles with FA (ZnONPs-FA) to act on hepatoma Huh-7 and HepG2 cells. The results showed that ZnONPs-FA could induce oxidative DNA damage and apoptosis by inducing ROS production.
JAK2↓, by inhibiting the JAK2/STAT6 immune signaling pathway
STAT6↓,
NF-kB↓, thus inhibiting the activation of NF-κB
PYCR1↓, FA can target PYCR1 and inhibit its enzyme activity in a concentration-dependent manner.
PI3K↓, FA inhibits the activation of the PI3K/AKT pathway
Akt↓,
mTOR↓, FA could significantly reduce the expression level of mTOR mRNA and Ki-67 protein in A549 lung cancer graft tissue
Ki-67↓,
VEGF↓,
FGFR1↓, FA is a novel FGFR1 inhibitor
EMT↓, FA can inhibit EMT
CAIX↓, selectively inhibit CAIX
LC3II↑, Autophagy vacuoles and increased LC3-II and p62 autophagy proteins were observed after treatment with this compound
p62↑,
PKM2↓, FA could inhibit the expression of PKM2 and block aerobic glycolysis
Glycolysis↓,
*BioAv↓, FA has poor solubility in water and a poor ability to pass through biological barriers [118]; therefore, the extent to which it is metabolized in vivo after oral administration is largely unknown

6857-

FBZ,

Fenbendazole induces pyroptosis in breast cancer cells through HK2/caspase-3/GSDME signaling pathway

vitro+vivo,

BC,

FBZ on mouse mammary carcinoma cells in vitro

tumCV↓, In vitro, FBZ dose - dependently inhibited cell viability
Pyro↑, upregulated pyroptosis markers (cleaved caspase - 3, GSDME - NT, IL - 1β),
cl‑Casp3↑,
GSDME↑,
IL1β↑,
Glycolysis↓, suppressed glycolysis by downregulating HK2.
HK2↓,
TumVol↓, In vivo, FBZ treatment significantly reduced tumor volume and weight, with minimal systemic toxicity.
TumW↓,
toxicity↓,

6982-

Form,

Formononetin: A Review of Its Anticancer Potentials and Mechanisms

Review,

Var,

AntiTum↑, Formononetin elicits antitumorigenic properties in vitro and in vivo by modulating numerous signaling pathways to induce cell apoptosis (by intrinsic pathway involving Bax, Bcl-2, and caspase-3 proteins)
Apoptosis↑,
BAX↑,
Bcl-2↓,
Casp3↑,
TumCCA↑, cell cycle arrest (by regulating mediators like cyclin A, cyclin B1, and cyclin D1),
cycA1/CCNA1↓,
CycB/CCNB1↓,
cycD1/CCND1↓,
TumCP↓, suppress cell proliferation [by signal transducer and activator of transcription (STAT) activation, phosphatidylinositol 3-kinase/protein kinase-B (PI3K/AKT), and mitogen-activated protein kinase (MAPK) signaling pathway],
VEGF↓, inhibit cell invasion [by regulating growth factors vascular endothelial growth factor (VEGF) and Fibroblast growth factor 2 (FGF2), and matrix metalloproteinase (MMP)-2 and MMP-9 proteins].
FGF↓,
MMP2↓,
MMP9↓,
eff↑, Co-treatment with other chemotherapy drugs such as bortezomib, LY2940002, U0126, sunitinib, epirubicin, doxorubicin, temozolomide, and metformin enhances the anticancer potential of both formononetin and the respective drugs through synergistic effec
ChemoSen↑,
chemoPv↑, Compiling the evidence thus far highlights the potential of formononetin to be a promising candidate for chemoprevention and chemotherapy.
p‑Akt↓, downregulation of EphB3, p-AKT, p-P13K, p-STAT3, inhibition of cyclin D1, MMP2/9
p‑STAT3↑,
TumCMig↓, MDA-MB-231-luc and 4T1 Inhibition of cell migration and invasion, elevation of TIMP-1 and TIMP-2, and suppression of PI3K/AKT signaling
TumCI↓,
TIMP1↑,
TIMP2↑,
PI3K↓,
Akt↓,
Dose↝, formononetin is administered into the mice intraperitoneally or intragastrically, mainly at doses between 10 and 60 mg/kg for 2–3 weeks via intraperitoneal route and between 15 and 100 mg/kg for more than a month via intragastric route
TumCG↓, In general, the formononetin treatment suppresses xenograft tumor growth in terms of tumor weight and volume, and also inhibits tumor invasiveness and angiogenesis.
TumW↓,
TumVol↓,
angioG↓,
Casp3↑, After exposure to formononetin, expression levels of cleaved caspase-3 and -9 in ovarian cancer cells increased in a dose-dependent manner
Casp9↑,
cl‑PARP↑, leading to the cleavage of poly(ADP-ribose) polymerase (PARP), which results in the inability to repair damaged DNA
DNArepair↓,
MMP↓, significant loss of mitochondrial membrane potential of approximately 457% (P < 0.001) and 265% (P < 0.001) in ES2 and OV90 ovarian cancer cells was observed upon exposure to 40 µM formononetin
BAX↑, expression of Bax protein surged upon formononetin treatment, while Bcl-2 protein level decreased
Bcl-2↓,
DR5↑, formononetin displayed high affinity and steric compatibility to death receptor 5, which could be activated to mediate the TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis
ROS↑, Formononetin can also induce the apoptotic pathway via the overexpression of reactive oxygen species (ROS) and disturbance of the intracellular antioxidant system.
eff↓, abrogated with the use of antioxidants such as N-acetyl-L-cysteine (NAC) and glutathione (GSH), suggesting that formononetin induces apoptosis via ROS production.
p‑ERK↓, formononetin was demonstrated to be a promising molecule that inhibits the phosphorylation of ERK1/2 itself as well as the phosphorylation of downstream ERK substrate (P90RSK)
PTEN↑, Besides the inhibition on AKT activity, formononetin upregulated PTEN expression in bladder cancer T24 cell.
Hif1a↓, The inhibition of AKT pathway by formononetin was mediated through the attenuation of HIF-α expression and inflammatory cytokines release
eff↑, Formononetin was shown to potentiate bortezomib-induced apoptosis in multiple myeloma
eff↑, synergistic effect was evident between formononetin and metformin in cancer treatment.
ChemoSen↑, sensitivity of glioma cells towards doxorubicin was shown to be enhanced by co-treatment with formononetin
HDAC↓, formononetin in doxorubicin-treated glioma cells was associated with formononetin’s suppressive effect on the histone deacetylase (HDAC) 5 expression
*BioAv↑, Due to its lipophilic nature, formononetin is rapidly absorbed into the gut via passive diffusion, with a peak absorption at 30 min ().
*Half-Life↝, Formononetin was determined to have a half-life of ∼2–3 h after oral administration and ∼2 h after intravenous administration
*BioAv↝, At oral administration of formononetin at 20–50 mg/kg, the peak plasma concentration was achieved between (Tmax) 0.5–1 h, while the maximum plasma concentration (Cmax) was determined ranging from 62 nM (17 ng/ml) to 302 nM (81 ng/ml).
*BioAv↑, Meanwhile, the Cmax of 1,302.8 nM (349.5 ng/ml) and 16,956.6 nM (4,548.5 ng/ml) was achieved after intravenous administration of formononetin at 4 and 10 mg/kg, respectively
*BioAv↑, rapidly metabolized and extensively converted into its metabolites daidzein and conjugates of daidzein and formononetin to be excreted, which makes it poorly bioavailable.
*eff↑, Drug delivery systems are strategies employed to overcome the low bioavailability and low water solubility of formononetin to achieve its pharmacological efficacy at minimum dose

948-

Fuc,

Low Molecular Weight Fucoidan Inhibits Tumor Angiogenesis through Downregulation of HIF-1/VEGF Signaling under Hypoxia

vitro+vivo,

Bladder,

T24/HTB-9

80-300mg/kg/day

mice

in-vitro,

Nor,

HUVECs

p‑PI3k/Akt/mTOR↓,
p‑p70S6↓,
p‑4E-BP1↓,
angioG↓, did not affect angiogenesis under normoxic conditions (data not shown), suggesting the antiangiogenic activity of LMWF is hypoxia specific.
Hif1a↓,
VEGF↑,
TumCG↓,
TumVol↓, in mice (needed 300mg/kg/day to actually shrink tumor as opposed to slowing growth)
TumW↓, in mice
Iron∅, maintaining Fe2+ availability through suppression of hypoxia-induced ROS formation is crucial for promoting HIF-1 degradation and diminishing HIF-1 activity by preventing PHD and FIH inactivation
ROS↓, LMWF may target different levels, including inhibition of ROS formation

7041-

GA,

Gallic acid suppresses the progression of clear cell renal cell carcinoma through inducing autophagy via the PI3K/Akt/Atg16L1 signaling pathway

vitro+vivo,

RCC,

786-O

in-vitro,

RCC,

ACHN

in-vitro,

Nor,

HK-2

selectivity↑, GA had a more potent viability inhibitory effect on ccRCC cells (786-O and ACHN) than the effect on normal renal tubular epithelial cell (HK-2), which demonstrated that GA selectively inhibits the viability of cancer cells.
TumCP↓, GA dose-dependently inhibited the proliferation, migration and invasion of ccRCC cells in vitro and in vivo.
TumCMig↓,
TumCI↓,
TumCCA↑, GA blocks the cycle process of ccRCC cells
TumVol↓, Moreover, the weight and volume of tumors were significantly lighter and smaller in the GA-treated group than in the control group
TumW↓,
Ki-67↓, significant decrease in the expression of Ki-67 (a marker of proliferation) and MMP-9 (a marker of metastasis) in the GA-treated group compared with the control group
MMP9↓,
TumAuto↑, GA induces autophagy in ccRCC
LC3B-II↓, LC3B-II and Beclin-1 protein expression was significantly decreased and P62 protein expression was significantly increased in the GA (IC50) + 3-MA treatment group compared with the GA (IC50) group
Beclin-1↓,
p62↑,

7137-

GI,

6-Shogaol from dried ginger inhibits growth of prostate cancer cells both in vitro and in vivo through inhibition of STAT3 and NF-κB signaling

in-vitro,

Pca,

LNCaP

in-vitro,

Pca,

DU145

in-vitro,

Pca,

PC3

vitro+vivo,

Pca,

HMVP2

STAT3↓, Mechanistic studies revealed that 6-SHO reduced constitutive and interleukin (IL)-6-induced STAT3 activation and inhibited both constitutive and TNF-α-induced NF-κB activity in these cells.
TNF-α↓,
NF-kB↓,
cycD1/CCND1↓, 6-SHO decreased the level of several STAT3 and NF-κB-regulated target genes at the protein level, including cyclin D1, survivin, and cMyc
survivin↓,
cMyc↓,
IL7↓, modulated mRNA levels of chemokine, cytokine, cell cycle, and apoptosis regulatory genes (IL-7, CCL5, BAX, BCL2, p21, and p27)
RANTES↓, 6-SHO decreased the mRNA expression of IL-7 and CCL5 in both DU145 and LNCaP cells.
BAX↑,
Bcl-2↓,
P21↑, 6-SHO increased the expression of p21, p27, SOCS1 and IRF1
p27/CDKN1B↑,
SOCS1↑,
IRF1↑,
eff↑, these results demonstrate that 6-GIN and 6-PAR have the ability to block growth and reduce survival of both human and mouse PCa cells but that they are both less potent than 6-SHO
TumVol↓, treatment with 6-SHO produced statistically significant decreases in tumor volume at both the 50 and 100 mg/kg doses (62% and 73%, respectively; p<0.05)
TumW↓, tumor weights were also reduced at both doses of 6-SHO (48% and 65% reduction, respectively)
toxicity↓, Taken together, these data demonstrate that 6-SHO has potent in vivo antitumor activity at the doses tested and is free of apparent adverse effects.

7245-

Gink,

Ginkgetin inhibits the growth of DU-145 prostate cancer cells through inhibition of signal transducer and activator of transcription 3 activity

vitro+vivo,

Pca,

DU145

in-vitro,

CRC,

HCT116

in-vitro,

Nor,

MCF10

STAT3↓, Ginkgetin inhibited both inducible and constitutively activated STAT3 and blocked the nuclear translocation of p-STAT3 in DU-145 prostate cancer cells.
cycD1/CCND1↓, leading to the inhibition of expression of STAT3 target genes such as cell survival-related genes (cyclin D1 and survivin) and anti-apoptotic proteins (Bcl-2 and Bcl-xL).
survivin↓,
Bcl-2↓,
Bcl-xL↓,
TumCG↓, We also found that ginkgetin inhibited tumor growth in xenografted nude mice and downregulated p-STAT3Tyr705 and survivin in tumor tissues.
Dose↝, ginkgetin and its derivatives at 5 and 10 μM, only ginkgetin downregulated the phosphorylation of STAT3
TumCCA↑, Ginkgetin causes accumulation of cells in the G0/G1 phase of the cell cycle and induces apoptosis
Apoptosis↑,
TumVol↓, Therefore, ginkgetin reduces tumor volume and tumor weight in the nude mouse xenograft by inhibiting p-STAT3.
TumW↓,

7260-

Gink,

Ginkgetin: A natural biflavone with versatile pharmacological activities

Review,

Var,

Review,

Stroke,

Review,

AD,

*AntiCan↑, Ginkgetin (GK), a natural non-toxic biflavone, has been shown to exhibit anti-cancer, anti-inflammatory, anti-microbial, anti-adipogenic, and neuroprotective activities.
*Inflam↓,
*AntiBio↑,
*neuroP↑,
*TumCCA↑, GK combats cancer progression by arresting cell cycle, inducing apoptosis, stimulating autophagy, and targeting many deregulated signaling pathways such as JAK/STAT and MAPKs.
Apoptosis↑,
TumAuto↑,
iNOS↓, GKhalts inflammation mediators like interleukins, iNOS, COX-2, PGE2, NF-κB, and acts as an inhibitor of PLA2
COX2/PTGS2↓,
PGE2↓,
NF-kB↓,
PLA2↓,
*neuroP↑, GK shows strong neuroprotection against oxidative stress-promoted cell death, inhibits cerebral micro-hemorrhage, decreases neurologic deficits, and halts apoptosis of neurons
*Stroke↓, in cerebral ischemia rat model, GK significantly improved I/R-stimulated neurological deficit scores
*AntiFungal↓, GK also acts as anti-fungal, anti-viral, anti-bacterial, leishmanicidal and anti-plasmodial agent.
*Bacteria↓,
Bcl-xL↓, steosarcoma cells, GK significantly suppressed the levels of B-cell lymphoma-extra-large (Bcl-xL) and B-cell lymphoma 2 (Bcl-2) proteins while significantly elevated levels of caspase-9 and -3 along with cleaved poly ADP ribose polymerase (PARP)
Bcl-2↓,
Casp9↑,
Casp3↑,
cl‑PARP↑,
IL6↓, GK selectively repressed the proliferation of prostate tumor via repressing interleukin 6 (IL-6)-induced as well as constitutive activation of STAT3
STAT3↓,
JAK1↓, GK abrogated the constitutive activation of both Src and JAK1 kinases which in turn halted STAT3 activation in FaDu and A549 cells.
survivin↓, suppressed its target genes including survivin, cyclooxygenase-2 (COX-2), inhibitor of apoptosis protein-1 (IAP-1), Bcl-xL, Bcl-2, matrix metalloproteinase 2 and 9 (MMP-2 and -9)
COX2/PTGS2↓,
IAP1↓,
MMP2↓,
MMP9↓,
PTEN↑, GK prompted the mRNA and protein expression of phosphatase and tensin homolog (PTEN) and SHP-1 which also paly role in STAT3 activation
SHP1↑,
eff↑, When GK is applied in combination with resveratrol, they synergistically act to suppress endothelial cell proliferation, migration, and reactive oxygen species (ROS) production as compared to mono drug
TumVol↓, GK decreased the weight and volume of tumor by 67.4% and 65.6%, respectively in the DU-145 xenografted mice model as compared to control and no toxic effect towards normal cells had been observed
TumW↓,
*toxicity↓,
*ROS↓, mediated neuronal cell damage in vitro by reducing intracellular ROS and maintaining MMP

7281-

Gins,

Inhibiting PI3K-AKt signaling pathway is involved in antitumor effects of ginsenoside Rg3 in lung cancer cell

vitro+vivo,

Lung,

A549

 In vivo, A549，H23 cells were subcutaneously injected into the nude mice.

vitro+vivo,

Lung,

H23

PI3K↓, Rg3 obviously inhibited cell viability, induced apoptosis and inhibited PI3K/Akt signalling pathway on A549, H23 cells in vitro and in vivo.
Akt↓,
TumW↓, Rg3 effectively inhibited the volume and weight of tumor in xenografts model, which may be related with inhibiting PI3K/Akt signaling pathways.
TumVol↓,

7489-

H2,

Molecular Hydrogen in the Treatment of Respiratory Diseases

Review,

Asthma,

*antiOx↑, Molecular hydrogen is gaining increasing attention as an antioxidant, anti-inflammatory, and antiapoptotic agent.
*Inflam↓,
*Apoptosis↓,
*Dose↓, It reaches a maximum level of about 0.78 mM (≈1.6 mg/L) at room temperature with a loss of about 2–5% per 3 min
*Dose↝, It is produced (and consumed) by bacteria of the gut microbiota .The most prominent bacterial phyla involved in this process are the Firmicutes and Bacteroidetes phyla, which include the anaerobic Clostridium species
*eff↑, hydrogen mixed with oxygen at a ratio of 96%-to-4%, known as the Hydrox gas mixture, was used by deep-sea divers to prevent decompression sickness and allow diving to depths of up to 500 m
*ROS↓, The antioxidant activity of H2 is based on two processes: a direct scavenging of the most toxic reactive oxygen and nitrogen species (ROS/RNS),
*RNS↓,
*NRF2↑, H2 activates the Nrf2 (nuclear factor erythroid 2-related factor 2) pathway, a key transcription factor involved in oxidative stress-related responses, including cytoprotective, antioxidant, and detoxifying enzymes such as HO-1
*HO-1↑,
*Fenton↓, removal of free heme and inhibition of the Fenton reaction
*NLRP3↓, the activation of the Nrf2 pathway has been shown to inhibit the NLRP3 (NLR family pyrin domain containing 3) inflammasome,
*NADPH↓, H2 suppresses the activation of the NADPH oxidase pathway and downregulates the expression of NOX2 and NOX4
*NOX4↓,
*NOX↓,
*MPO↓, H2 has been shown to reduce the overactivation of myeloperoxidase (MPO)
*NF-kB↓, would further suppress the NFκB
*TNF-α↓, figure 3
*IL6↓,
*IL1β↓,
*HMGB1↓,
*IL4↑,
*IL10↑,
*M2 MC↑, Additionally, H2 promotes the polarization of macrophages from the proinflammatory M1 type to the anti-inflammatory M2 type
*Treg lymp↝, It also inhibits Th2 responses, restores regulatory T cells (Treg), and, thus, normalizes an overactivated immune system
*Bcl-2↑, upregulate the antiapoptotic factors, including Bcl-2 and Bcl-xl.
*Bcl-xL↑,
*PI3K↑, phenomenon is likely facilitated by the activation of the PI3K/Akt and JAK2/STAT3 signaling pathways
*Akt↑,
*JAK2↑,
*STAT3↑,
*Dose↑, The consumption of certain prebiotics, especially those rich in dietary fiber, indigestible starches, and sugars (lactulose), has been demonstrated to enhance intestinal H2 production through the activity of intestinal flora
*CD4+↑, H2 increased the population of CD4+CD25+Foxp3+ Treg cells, which are often decreased in allergic rhinitis (AR)
*CD25+↑,
*FOXP3↑,
*MDA↓, H2 administration attenuated oxidative stress expressed as lower MDA and other lipid peroxidation markers along with an enhancement in the expression and activity of endogenous antioxidant enzymes such as SOD or CAT
*SOD↑,
*Catalase↑,
*Casp3↓, inhibition of proapoptotic processes like the caspase 3 and 9 pathways
*Casp9↓,
*TBARS↓, drinking of HRW by patients with asthma and COPD leads to an increase in blood oxygen saturation, vitamin E levels, along with lower oxidative stress markers such as thiobarbituric acid reactive substances (TBARS), MDA,
*SpO2↑,
*VitE↓,
*OS↑, COPD:In general, H2 administration has been found to lead to enhanced survival and reduced weight loss [110], improved lung function and static lung compliance, and decreased arterial blood pressure
*Weight↑,
*DNAdam↓, reduction in levels of oxidative DNA damage markers
*PGE2↓, H2 reduced elevated inflammatory markers, including IL-1β, IL-6, TNF-α, prostaglandin E2 (PGE2) [29,65,71,128,130], macrophage protein 1α 2 (MP1α), and monocyte chemoattractant protein-1 (MCP-1)
*MCP1/CCL2↓,
*lipid-P↓, Further, a reduction in oxidative stress markers such as lipid peroxidation and proapoptotic markers, including Bax and caspase-3, was observed.
*TumCP↓, H2-rich medium reduced the colony size and formation of tongue cancer cells and decreased proliferation in human fibrosarcoma and esophageal cancer cells, as well as A549 cells
*tumCV↓, decrease in cell viability, migration, and invasion
*TumCMig↓,
*TumCI↓,
TumW↓, A reduction in tumor weight and size, as well as a lower number of cells of squamous cell carcinoma, was revealed by animal studies.
TumVol↓,
selectivity↑, Notably, as previously reported, H2 administration exhibited no effect on healthy animals or non-cancerous cell lines
QoL↑, Patients reported improved quality of life with better physical status and fewer pulmonary symptoms
ChemoSen↑, In combination with conventional (such as cis-platin) and modern (including antibodies like nivolumab) therapeutics, H2 enhanced drug activity, resulting in enhanced outcomes and improved disease control
chemoP↑, and reduced side effects of the treatment, such as nephrotoxicity, weight loss, insomnia, pain, or hearing loss in the case of radiotherapy
radioP↑, radioprotective effects of H2 are primarily attributed to its hydroxyl radical scavenging activity
ROS↑, As indicated by Yang et al., the latter include the activation of the ROS/NLRP3/caspase-3/gasdermin D-mediated pyroptotic pathways
NLRP3↑,
Casp3↑,
VEGF↓, suppression of vascular endothelial growth factor (VEGF) expression
Wnt↓, H2 result in the suppression of the overactivated Wnt/beta-catenin signaling pathways, which further leads to suppression of tumor progression
β-catenin/ZEB1↓,

2509-

H2,

Hydrogen inhibits endometrial cancer growth via a ROS/NLRP3/caspase-1/GSDMD-mediated pyroptotic pathway

in-vitro,

Endo,

AN3CA

in-vivo,

Endo,

endometrial tumors in a xenograft mouse model.

selectivity↑, Hydrogen exerts a biphasic effect on cancer by promoting tumor cell death and protecting normal cells, which might initiate GSDMD pathway-mediated pyroptosis.
mt-ROS↑, We therefore concluded that molecular hydrogen activated ROS and mtROS generation in endometrial cancer cells.
ROS↑,
TumW↓,
GSDMD↑, ability of hydrogen to stimulate NLRP3 inflammasome/GSDMD activation in pyroptosis
Pyro↑,
Dose↝, Hydrogenated water was produced by H2 dissolved in water saturantly under 0.4 MPa pressure for 6 h with a concentration of 1.0 ppm produced by hydrogen water apparatus
eff↓, In contrast, NAC decreased ROS levels in hydrogen-treated endometrial cancer cells
TumVol↓, We demonstrated that drinking hydrogen-rich water reduced the volume of endometrial tumors in a xenograft mouse model.

7370-

HibSad,

Hibiscus sabdariffa leaf induces apoptosis of human prostate cancer cells in vitro and in vivo

vitro+vivo,

Pca,

LNCaP

n xenograft tumour studies.

in-vitro,

Pca,

PC3

in-vitro,

Pca,

DU145

eff↑, among three kinds of human prostate cancer (CaP) cells, androgen-dependent LNCaP cells were the most susceptible to HLE.
Dose↝, fed with 5 g of daily basal diets containing 50 (1.0%) or 100 (2.0%) lg mL1 (w/v) HLE for 90 days,
Bcl-2↓, protein expressions of Bcl-2 and Mcl-1 were decreased to about 80% and 60% after treatment with 2.5 mg/mL of HLE for 24 h
Mcl-1↓,
BAX↑, translocation of Bax to the mitochondria increased to 2.75-fold
Cyt‑c↑, cytochrome c was released from mitochondria to cytosol (Fig. 3B), indicating activation of the intrinsic pathway.
FasL↑, FasL expression increased to about 2.15- and 1.5-fold of control after HLE (2.5 mg/mL) and EA (100 lM) exposure for 24 h.
eff↑, The greatest inhibition was seen in androgen-dependent LNCaP cells compared to PC3 and DU145
TumW↓, treatment with 2% HLE resulted in the almost complete inhibition of tumour incidence, tumour weight and tumour volumne.
TumVol↓,
other↝, The calyces of the Hibiscus flowers are used to prepare hot (sour tea) and cold beverages that are consumed worldwide.

2073-

HNK,

Honokiol induces apoptosis and autophagy via the ROS/ERK1/2 signaling pathway in human osteosarcoma cells in vitro and in vivo

in-vitro,

OS,

U2OS

21.5 μM

in-vivo,

NA,

40 mg/kg

TumCD↑, honokiol caused dose-dependent and time-dependent cell death in human osteosarcoma cells
TumAuto↑, death induced by honokiol were primarily autophagy and apoptosis.
Apoptosis↑,
TumCCA↑, honokiol induced G0/G1 phase arrest,
GRP78/BiP↑, elevated the levels of glucose-regulated protein (GRP)−78, an endoplasmic reticular stress (ERS)-associated protein
ROS↑, increased the production of intracellular reactive oxygen species (ROS)
eff↓, In contrast, reducing production of intracellular ROS using N-acetylcysteine, a scavenger of ROS, concurrently suppressed honokiol-induced cellular apoptosis, autophagy, and cell cycle arrest.
p‑ERK↑, honokiol stimulated phosphorylation of extracellular signal-regulated kinase (ERK)1/2.
selectivity↑, human fibroblasts showed strong resistance to HNK, the IC50 values for which were 118.9 and 71.5 μM
Ca+2↑, HNK increased intracellular Ca2+ in both HOS and U2OS cells
MMP↓, mitochondrial membrane potential (MMP) sharply decreased following HNK treatment
Casp3↑, HNK markedly activated caspase-3, caspase-9
Casp9↑,
cl‑PARP↑, led to PARP cleavage
Bcl-2↓, expression of Bcl-2, Bcl-xl, and survivin was found to be decreased
Bcl-xL↓,
survivin↓,
LC3B-II↑, HNK increased the level of LC3B-II and Atg5 in HOS and U2OS cells.
ATG5↑,
TumVol↓, HNK at doses of 40 mg/kg resulted in significant decrease in tumor volume and weight, after 7 days of drug administration
TumW↓,
ER Stress↑, ER stress can trigger ROS production through release of calcium

2081-

HNK,

Honokiol induces ferroptosis in colon cancer cells by regulating GPX4 activity

in-vitro,

Colon,

RKO

11.42 μM

in-vitro,

Colon,

HCT116

47.65 μM

in-vitro,

Colon,

SW48

in-vitro,

Colon,

HT-29

in-vitro,

Colon,

LS174T

in-vitro,

Colon,

HCT8

in-vitro,

Colon,

SW480

in-vivo,

NA,

mice

tumCV↓, HNK reduced the viability of CC cell lines by increasing ROS and Fe2+ levels
ROS↑, observations suggest that ROS production is a determining factor of HNK cytotoxicity. exact mechanism underlying the pro-oxidant activity of HNK is unclear in CC
Iron↑,
GPx4↓, HNK decreased the activity of Glutathione Peroxidase 4 (GPX4)
mtDam↑, intracellular mitochondria decreased, the membrane density increased, the mitochondrial ridge shrank or disappeared, and the bilayer membrane density increased.
Ferroptosis↑, results suggested that GPX4 may be the key molecule that regulates HNK-induced ferroptosis in CC cells
TumVol↓, tumor volumes and weights were significantly lower in the Lv-NC group than in the Lv-GPX4 group
TumW↓,

7569-

HYP,

Inhibitory effects of hyperoside on lung cancer by inducing apoptosis and suppressing inflammatory response via caspase-3 and NF-κB signaling pathway

vitro+vivo,

Lung,

A549

nude mice

TumCP↓, Our results showed that hyperoside suppressed the proliferation, migration and invasion.
TumCMig↓,
TumCI↓,
Casp3↑, apoptosis was induced by hyperoside via Bcl-2/Bax-regulated Caspase3 activation, suggesting that hyperoside might inhibit lung cancer progression through apoptotic induction.
Apoptosis↑,
NF-kB↓, through inactivating NF-κB signaling pathway
TNF-α↓, Subsequently, inflammatory cytokines, including TNF-α, IL-6, IL-1β and IL-18, were down-regulated significantly.
IL6↓,
IL1β↓,
IL18↓,
TumVol↓, tumor volume and weight were reduced after hyperoside administration
TumW↓,

7590-

I3C,

Indole-3-carbinol synergistically sensitises ovarian cancer Indole-3-carbinol synergistically sensitises ovarian cancer cells to bortezomib treatmentcells to bortezomib treatment

in-vivo,

Ovarian,

ChemoSen↑, I3C sensitised ovarian cancer cell lines to bortezomib treatment through potent synergistic mechanisms. Moreover, I3C and bortezomib co-treatment sensitised ovarian cancer cells to the standard chemotherapeutic agents, cisplatin and carboplatin.
TumCG↓, co-treatment with I3C and bortezomib significantly inhibited tumour growth and reduced tumour weight compared with either drug alone.
TumW↓,

7776-

IBC,

Isobavachalcone Activates Antitumor Immunity on Orthotopic Pancreatic Cancer Model: A Screening and Validation

vitro+vivo,

PC,

Panc02

TumCP↓, IBC could inhibit Panc 02 cell proliferation and induce apoptosis via increasing the production of reactive oxygen species.
Apoptosis↑,
ROS↑,
TumW↓, IBC could attenuate the weight of solid tumors, increase CD8+ T cells, and reduce M2 macrophages in the tumor tissue and spleen
CD8+↑,
M2 MC↓,
CSCs↓, IBC alleviated the proportion of myeloid-derived suppressor cells (MDSCs) in the tumor tissue but had no change in the spleen.
antiNeop↑, IBC as an antineoplastic agent, which could attenuate the growth of pancreatic cancer via activating the immune activity
Imm↑,
eff↓, NAC pretreatment abrogated apoptosis produced by IBC in Panc 02 cells.
Bcl-2↓, IBC could decrease the expression of Bcl-2 and increase expression of Bax
BAX↑,

Showing Research Papers: 1 to 50 of 73
Page 1 of 2 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 73

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome(tgid=24) ⓘ

CD8+↑, 1,
Total Targets: 266

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

AntiBio↑, 1, NLR↓, 1, SpO2↑, 1, Stroke↓, 1,

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1, Catalase↑, 1, Fenton↓, 1, HO-1↑, 1, lipid-P↓, 1, MDA↓, 1, MPO↓, 1, NOX4↓, 1, NRF2↑, 1, RNS↓, 1, ROS↓, 2, SOD↑, 1, TBARS↓, 1, VitE↓, 1,

Core Metabolism/Glycolysis(tgid=4) ⓘ

NADPH↓, 1,

Cell Death(tgid=5) ⓘ

Akt↑, 1, Apoptosis↓, 1, Bcl-2↑, 1, Bcl-xL↑, 1, Casp3↓, 1, Casp9↓, 1,

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

PI3K↑, 1, STAT3↑, 1,

Migration(tgid=13) ⓘ

Treg lymp↝, 1, TumCI↓, 1, TumCMig↓, 1, TumCP↓, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD14↑, 1, CD25+↑, 1, CD4+↑, 1, FOXP3↑, 1, HMGB1↓, 1, IFN-γ↑, 1, IL10↑, 2, IL1β↓, 1, IL4↑, 2, IL6↓, 1, Inflam↓, 2, JAK2↑, 1, M2 MC↑, 1, MCP1/CCL2↓, 1, NF-kB↓, 1, PGE2↓, 1, TNF-α↓, 1, TNF-α↑, 1,

Cellular Microenvironment(tgid=17) ⓘ

NOX↓, 1,

Protein Aggregation(tgid=19) ⓘ

NLRP3↓, 1,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1, BioAv↑, 3, BioAv↝, 1, Dose↓, 1, Dose↑, 1, Dose↝, 1, eff↑, 2, Half-Life↝, 1,

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1, neuroP↑, 2, OS↑, 1, toxicity↓, 2, toxicity↝, 1, Weight↑, 1,

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↓, 1, Bacteria↓, 1,
Total Targets: 71

Scientific Paper Hit Count for: TumW, Tumor Weight

5 Apigenin (mainly Parsley)
4 IP6 (Inositol 1,2,3,4,5,6-hexakisphosphate)
3 EGCG (Epigallocatechin Gallate)
3 Sulforaphane (mainly Broccoli)
3 Shikonin
2 cetuximab
2 Metformin
2 Ashwagandha(Withaferin A)
2 Chlorogenic acid
2 immunotherapy
2 Dichloroacetate
2 Chemotherapy
2 Ferulic acid
2 Ginkgetin
2 Hydrogen Gas
2 Honokiol
2 Inositol
2 Piperlongumine
1 3-bromopyruvate
1 Allicin (mainly Garlic)
1 Andrographis
1 Aspirin
1 Baicalein
1 borneol
1 Carvacrol
1 Cannabidiol
1 Celastrol
1 chaetocin
1 chitosan
1 Chrysin
1 Cinnamon
1 Curcumin
1 Cynaropicrin
1 Bortezomib
1 Diclofenac
1 Docosahexaenoic Acid
1 Evodiamine
1 Fenbendazole
1 Formononetin
1 Fucoidan
1 Gallic acid
1 Ginger/6-Shogaol/Gingerol
1 Ginseng
1 Hibiscus sabdariffa
1 Hyperoside
1 Indole-3-carbinol
1 Isobavachalcone
1 Inulin Prebiotic
1 capecitabine
1 Isovitexin
1 Linalool
1 Lycopene
1 Naringin
1 Propolis -bee glue
1 Phenethyl isothiocyanate
1 Pterostilbene
1 Resveratrol
1 Cisplatin
1 Selenite (Sodium)
1 Terpinen-4-ol / Tea Tree Oil
1 Aflavin-3,3′-digallate

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:915  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

TumW Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Metal & Cofactor Biology(tgid=2) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Cellular Microenvironment(tgid=17) ⓘ

Protein Aggregation(tgid=19) ⓘ

Hormonal & Nuclear Receptors(tgid=20) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Cellular Microenvironment(tgid=17) ⓘ

Protein Aggregation(tgid=19) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

Home Page