TumVol Cancer Research Results

TumVol, Tumor Volume: Click to Expand ⟱

Source:

Type:

Tumor Volume

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↑, 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↑,

5975-

AgNPs,

PDT,

CDT,

RF,

Recent Advances in the Application of Silver Nanoparticles for Enhancing Phototherapy Outcomes

Review,

Var,

Review,

BPH,

ROS↑, capacity of these nanostructures to release silver ions (Ag+) and enhance the production of reactive oxygen species (ROS) has been explored in combination with light to treat several diseases.
EPR↓, Furthermore, the use of NPs in biomedical applications takes advantage of the enhanced permeability and retention (EPR) effect, a phenomenon that enables greater penetration and longer retention times in cancer cells compared to normal cells
eff↑, When the AgNPs are exposed to an electromagnetic field, the electrons in the metals’ conduction band oscillate collectively and in resonance with the light frequency, generating the LSPR at the AgNPs’ surface.
Bacteria↓, NPs have already been approved by the Food and Drug Administration (FDA) as antibacterial agents for clinical use [
eff↑, Smaller AgNPs have been appointed as having greater reactivity compared to larger ones, due to their higher surface area-to-volume ratio and enhanced cellular uptake.
eff↑, TSC-coated AgNPs exhibited stronger binding affinity to Gram-positive bacteria, while the positively charged AgNPs-TMA were more efficiently internalized by Gram-negative bacteria.
TumVol↓, After PTT treatment with a AgNPs-PVP dose of 50 mg.kg−1 for 5 min, the prostate size of the BPH-bearing animals was reduced compared with non-treated rats, showing that AgNPs could prevent the progression of BHP.

4394-

AgNPs,

Silver nanoparticles provoke apoptosis of Dalton's ascites lymphoma in vivo by mitochondria dependent and independent pathways

in-vivo,

lymphoma,

OS↑, Results indicate that the AgNPs were efficient in prolongation of life span, reduction of tumor volume and body weight in tumor animals.
TumVol↓,
Weight↑,
AntiTum↑, AgNPs are potent in antitumor activity and the molecular mechanism is by the induction of apoptosis through the mitochondrial dependent and independent pathways.
Apoptosis↑,
mtDam↑,

4431-

AgNPs,

doxoR,

Oxidative Stress-Induced Silver Nano-Carriers for Chemotherapy

in-vitro,

BC,

4T1

PA-AgNPs have an average hydrodynamic diameter of 130 nm

in-vivo,

BC,

4T1

in-vitro,

Nor,

3T3

AntiCan↑, AgNPs have been demonstrated to exhibit anti-tumor effects through cell apoptosis.
ROS↑, ox-carried PA-AgNPs generate reactive oxidation species intensively beside 4T1 cells.
TumVol↓, in vivo study confirms that PA-AgNPs with Dox successfully inhibit tumors, which are about four times smaller than the control group and have high biosafety that can be applied for chemotherapy.
EPR↑, While all normal cells need enough vitamins to survive, cancer cells require a considerable number of vitamins to proliferate rapidly. As a result, the receptors on the cancer cell surface are overexpressed to capture as many vitamins as possible.
selectivity↑, PA-AgNPs (without/with Dox) concentrations ranging from 0 to 100 μg mL−1 did not seem to impair 3T3 cell viability due to poor uptake by normal cells.
ChemoSen↑, These results suggested that Dox-carried PA-AgNPs were both safer and more effective for cancer prevention.

4361-

AgNPs,

GoldNP,

Biocompatible silver, gold and silver/gold alloy nanoparticles for enhanced cancer therapy: in vitro and in vivo perspectives

in-vivo,

Liver,

HepG2

IC50 values of the AgNPs, AuNPs and Ag/AuNPs on HepG2 cells were determined as 38.42 μg ml-1, 43.25 μg ml-1 and 39.20 μg ml-1

Sprague Dawley (SD) rat model

TumCD↑, IC50 values of the AgNPs, AuNPs and Ag/AuNPs on HepG2 cells were determined as 38.42 μg ml-1, 43.25 μg ml-1 and 39.20 μg ml-1
TumVol↓, tumour reduction (∼45 to 65%) was observed in the nanoparticle-treated animal
*toxicity↝, The No-Observed-Adverse-Effect-Level (NOAEL) for the AgNPs was determined to be 2000 mg per kg of body weight (bw) from an acute toxicity test.
hepatoP↑, (Ag/AuNPs) for hepatoprotective activity against diethylnitrosamine (DEN)-induced liver cancer in a Sprague Dawley (SD) rat model

4363-

AgNPs,

Immunomodulatory properties of silver nanoparticles contribute to anticancer strategy for murine fibrosarcoma

in-vivo,

fibroS,

particles was approximately 10 nm

LACA mice

TumVol↓, incidence and size of fibrosarcoma were reduced or delayed when murine fibrosarcoma groups were treated by AgNP-MSA
TNF-α↓, TNF-α, IL-6 and IL-1β these cytokines were found to be downregulated after treatment with AgNP-MSA
IL6↓,
IL1β↓,
*toxicity↝, liver sections were found to have normal architecture in all treated groups except those treated at the 9 and 10 mg/kg b.w. doses
TumCG↓, treatment with AgNPs, the logistic growth of the tumor incidence was significantly lower (
selectivity↑, MSA-AgNPs aggregated instantly in response to the acidic extracellular pH of solid tumors, leading to greatly enhanced uptake by cancer cells
selectivity↑, Because the particle size in the study was approximately 10 nm, any AgNP that escaped entry into the tumor microenvironment and entered the systemic circulation was effectively cleared from the body.
Weight↑, AgNP-MSA not only inhibited the tumor incidence but also helped to overcome the progressive body weight loss of tumor-bearing mice.
ROS↑, anticancer property demonstrated by AgNP can be attributed to this increase in oxidative stress in the tumor microenvironment.
NO↑, AgNPs significantly increased the oxygen free radical and NO levels in the tumor microenvironment, which oppose hypoxia.

312-

AgNPs,

wortm,

Inhibition of autophagy enhances the anticancer activity of silver nanoparticles

vitro+vivo,

Cerv,

HeLa

 10 μg/mL(10ppm)

 39.25 μg/mL

APA↑,
p62↓, decrease in the level of SQSTM1, similar to starvation treatment
PIK3CA↑, suggesting that Ag NPs induced autophagy by enhancing autophagosome formation through the PtdIns3K pathway.
TumVol↓, 61% decrease in tumor weight
TumAuto↑, Here we show that Ag NPs induced autophagy in cancer cells by activating the PtdIns3K signaling pathway.
eff↑, Inhibition of autophagy enhanced the antitumor efficacy of Ag NPs in a mouse model

362-

AgNPs,

Comparative and Mechanistic Study on the Anticancer Activity of Quinacrine-Based Silver and Gold Hybrid Nanoparticles in Head and Neck Cancer

vitro+vivo,

SCC,

SCC9

 0.5ug/mL

DNAdam↑,
TumVol↓, mice

378-

AgNPs,

Antitumor efficacy of silver nanoparticles reduced with β-D-glucose as neoadjuvant therapy to prevent tumor relapse in a mouse model of breast cancer

ex-vivo,

BC,

4T1

 8.1 μg/mL

TumVol↓,
TumMeta↓,
Ki-67↓,

390-

AgNPs,

Anti-cancerous effect of albumin coated silver nanoparticles on MDA-MB 231 human breast cancer cell line

in-vitro,

BC,

MDA-MB-231

5 μM

IC50 is 30x higher for normal white blood cells

in-vivo,

BC,

mice

ROS↑,
TumVol↓,

5342-

Ajoene,

The garlic-derived organosulfur component ajoene decreases basal cell carcinoma tumor size by inducing apoptosis

in-vivo,

BCC,

TumVol↓, We applied ajoene topically to the tumors of 21 patients with either nodular or superficial basal cell carcinoma (BCC). A reduction in tumor size was seen in 17 patients.
Bcl-2↓, Bcl-2 expression in a selection of these tumors before and after treatment showed a significant decrease in this apoptosis-suppressing protein.
Apoptosis↑, we conclude that ajoene can reduce BCC tumor size, mainly by inducing the mitochondria-dependent route of apoptosis.

546-

AL,

Effects of garlic intake on cancer: a systematic review of randomized clinical trials and cohort studies

Review,

NA,

Risk↓,
TumVol↓, significant decrease in the number and size of colorectal adenomas

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

271-

ALA,

VitC,

LDN,

The Long-Term Survival of a Patient With Stage IV Renal Cell Carcinoma Following an Integrative Treatment Approach Including the Intravenous α-Lipoic Acid/Low-Dose Naltrexone Protocol

OS↑, >9 years
Weight↑, up 30 lbs
TumVol↓, PET/CT scan

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↑,

1553-

Api,

Role of Apigenin in Cancer Prevention via the Induction of Apoptosis and Autophagy

Review,

NA,

Dose∅, oral administration of apigenin (20 and 50 μg/mice) for 20 weeks reduced tumor volumes
TumVol↓,
Dose∅, 15-week period of oral administration of apigenin (2.5 mg/kg) in hamsters resulted in reduction of tumor volume
COX2↓, topical application of apigenin (5 μM) prior to UVB-exposure attenuated the expression of COX-2 and hypoxia inducible factor (HIF)-1α,
Hif1a↓,
TumCCA↑, apigenin was capable to promote cell cycle arrest and induction of apoptosis through p53-related pathways
P53↑,
P21↑, induction of the cell cycle inhibitor p21/WAF1,
Casp3↑,
DNAdam↑, DNA fragmentation
TumAuto↝, Only a small number of studies have observed the induction of autophagy in response to apigenin and the results are controversial

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%

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↓,

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↓,

3391-

ART/DHA,

Antitumor Activity of Artemisinin and Its Derivatives: From a Well-Known Antimalarial Agent to a Potential Anticancer Drug

Review,

Var,

TumCP↓, inhibiting cancer proliferation, metastasis, and angiogenesis.
TumMeta↓,
angioG↓,
TumVol↓, reduces tumor volume and progression
BioAv↓, artemisinin has low solubility in water or oil, poor bioavailability, and a short half-life in vivo (~2.5 h)
Half-Life↓,
BioAv↑, semisynthetic derivatives of artemisinin such as artesunate, arteeter, artemether, and artemisone have been effectively used as antimalarials with good clinical efficacy and tolerability
eff↑, preloading of cancer cells with iron or iron-saturated holotransferrin (diferric transferrin) triggers artemisinin cytotoxicity
eff↓, Similarly, treatment with desferroxamine (DFO), an iron chelator, renders compounds inactive
ROS↑, ROS generation may contribute with the selective action of artemisinin on cancer cells.
selectivity↑, Tumor cells have enhanced vulnerability to ROS damage as they exhibit lower expression of antioxidant enzymes such as superoxide dismutase, catalase, and gluthatione peroxidase compared to that of normal cells
TumCCA↑, G2/M, decreased survivin
survivin↓,
BAX↑, Increased Bax, activation of caspase 3,8,9 Decreased Bc12, Cdc25B, cyclin B1, NF-κB
Casp3↓,
Casp8↑,
Casp9↑,
CDC25↓,
CycB/CCNB1↓,
NF-kB↓,
cycD1/CCND1↓, decreased cyclin D, E, CDK2-4, E2F1 Increased Cip 1/p21, Kip 1/p27
cycE/CCNE↓,
E2Fs↓,
P21↑,
p27↑,
ADP:ATP↑, Increased poly ADP-ribose polymerase Decreased MDM2
MDM2↓,
VEGF↓, Decreased VEGF
IL8↓, Decreased NF-κB DNA binding [74, 76] IL-8, COX2, MMP9
COX2↓,
MMP9↓,
ER Stress↓, ER stress, degradation of c-MYC
cMyc↓,
GRP78/BiP↑, Increased GRP78
DNAdam↑, DNA damage
AP-1↓, Decreased NF-κB, AP-1, Decreased activation of MMP2, MMP9, Decreased PKC α/Raf/ERK and JNK
MMP2↓,
PKCδ↓,
Raf↓,
ERK↓,
JNK↓,
PCNA↓, G2, decreased PCNA, cyclin B1, D1, E1 [82] CDK2-4, E2F1, DNA-PK, DNA-topo1, JNK VEGF
CDK2↓,
CDK4↓,
TOP2↓, Inhibition of topoisomerase II a
uPA↓, Decreased MMP2, transactivation of AP-1 [56, 88] NF-κB uPA promoter [88] MMP7
MMP7↓,
TIMP2↑, Increased TIMP2, Cdc42, E cadherin
Cdc42↑,
E-cadherin↑,

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↓,

1177-

Ash,

Withaferin A downregulates COX-2/NF-κB signaling and modulates MMP-2/9 in experimental endometriosis

in-vivo,

EC,

150 mg withaferin A treated EM-induced rats

rats

TumVol↓,
MMP2↓,
MMP9↓,
NF-kB↓,
COX2↓,
NO↓,
IL1β↓,
IL6↓,

1176-

Ash,

Metabolic Alterations in Mammary Cancer Prevention by Withaferin A in a Clinically Relevant Mouse Model

in-vivo,

NA,

mice

TumVol↓, lower by 94%
Apoptosis↑,
Glycolysis↓, reduced levels of glycolysis intermediates.
PKM2↓,
PGK1↓,
ALDOAiso2↓,

5499-

Ba,

Anti-cancer effects of baicalein in non-small cell lung cancer in-vitro and in-vivo

vitro+vivo,

Lung,

H460

A xenograft nude mouse model

vitro+vivo,

Lung,

A549

TumCP↓, Baicalein significantly decreased lung cancer proliferation in H-460 cells in a dose dependent manner.
Apoptosis↑, dose-dependent induction in apoptosis associated with decreased cellular f-actin content, an increase in nuclear condensation and an increase in mitochondrial mass potential was observed.
F-actin↓,
TumVol↓, baicalein significantly (p < 0.05) reduced tumour growth and prolonged survival.
OS↑,
12LOX↓, demonstrated reduced expression of both 12-lipoxygenase and VEGF proteins in baicalein-treated tumours, relative to untreated.
VEGF↓,
angioG↓, improves survival in-vivo, an effect that is at least partly mediated through effects on cell cycle and tumour angiogenesis.

2599-

Ba,

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

in-vitro,

BC,

MCF-7

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↓,

5551-

BBM,

Berbamine Suppresses the Progression of Bladder Cancer by Modulating the ROS/NF-κB Axis

vitro+vivo,

Bladder,

tumCV↓, our results showed that berbamine inhibited cell viability, colony formation, and proliferation.
TumCP↓,
TumCCA↑, Additionally, berbamine induced cell cycle arrest at S phase by a synergistic mechanism involving stimulation of P21 and P27 protein expression
P21↑,
p27↑,
cycD1/CCND1↓, as well as downregulation of CyclinD, CyclinA2, and CDK2 protein expression.
cycA1/CCNA1↓,
CDK2↓,
EMT↓, In addition to suppressing epithelial-mesenchymal transition (EMT), berbamine rearranged the cytoskeleton to inhibit cell metastasis.
TumMeta↓,
p65↓, Mechanistically, the expression of P65, P-P65, and P-IκBα was decreased upon berbamine treatment
p‑p65↓,
IKKα↓,
NF-kB↑, berbamine attenuated the malignant biological activities of BCa cells by inhibiting the NF-κB pathway.
ROS↑, More importantly, berbamine increased the intracellular reactive oxygen species (ROS) level through the downregulation of antioxidative genes such as Nrf2, HO-1, SOD2, and GPX-1.
NRF2↓,
HO-1↓,
SOD2↓,
GPx1↓,
Bax:Bcl2↑, increase in the ratio of Bax/Bcl-2.
TumVol↓, berbamine successfully inhibited tumor growth and blocked the NF-κB pathway in our xenograft model

940-

BBR,

Functional inhibition of lactate dehydrogenase suppresses pancreatic adenocarcinoma progression

vitro+vivo,

PC,

PANC1

33uM-62uM

253 patients who were treatment‐naive and pathologically diagnosed with pancreatic adenocarcinoma

in-vivo,

PC,

MIA PaCa-2

mouse

LDHA↓, berberine was selected as functional inhibitor of LDHA
lactateProd↓, berberine treatment significantly suppressed intracellular lactate content at 5 μΜ and 10 μΜ
AMPKα↓, suppressed AMPKa activation
TumVol↓,
Ki-67↓,

5176-

BBR,

Berberine regulates AMP-activated protein kinase signaling pathways and inhibits colon tumorigenesis in mice

vitro+vivo,

CRC,

HCT116

mice

in-vitro,

CRC,

SW480

in-vitro,

CRC,

LoVo

TumVol↓, berberine treated mice showed a 60% reduction in tumor number
Ki-67↓, Berberine also decreased AOM/DSS induced Ki-67 and COX-2 expression
COX2↓,
AMPK↑, Berberine activated AMP-activated protein kinase (AMPK), a major regulator of metabolic pathways, and inhibited mammalian target of rapamycin (mTOR),
mTOR↓, Berberine Inhibits mTOR Signaling in CRC Cells
NF-kB↓, Berberine inhibited Nuclear Factor kappa-B (NF-κB) activity, reduced the expression of cyclin D1 and survivin, induced phosphorylation of p53 and increased caspase-3 cleavage in vitro.
cycD1/CCND1↓,
survivin↓,
P53↑,
cl‑Casp3↑,
TumCP↓, berberine suppresses colon epithelial proliferation and tumorigenesis via AMPK dependent inhibition of mTOR activity and AMPK independent inhibition of NF-κB.
Inflam↓, Berberine Inhibits AOM/DSS-induced Inflammation and Proliferation
COX2↓, We found COX-2 expression to be significantly decreased in berberine treated animals on day 70
ACC↑, Berberine Activates AMPK and Acetyl-CoA Carboxylase (ACC) in CRC Cells

2717-

BetA,

Betulinic Acid Induces ROS-Dependent Apoptosis and S-Phase Arrest by Inhibiting the NF-κB Pathway in Human Multiple Myeloma

in-vitro,

Melanoma,

U266

10-40uM

in-vivo,

Melanoma,

Nude Mouse Xenograft Model

in-vitro,

Melanoma,

RPMI-8226

Apoptosis↑, BA mediated cytotoxicity in MM cells through apoptosis, S-phase arrest, mitochondrial membrane potential (MMP) collapse, and overwhelming reactive oxygen species (ROS) accumulation.
TumCCA↑, S-Phase Arrest in U266 Cells
MMP↓,
ROS↑, exhibited concentration-dependent increases in intracellular ROS
eff↓, ROS scavenger N-acetyl cysteine (NAC) effectively abated elevated ROS, the BA-induced apoptosis was partially reversed
NF-kB↓, BA resulted in marked inhibition of the aberrantly activated NF-κB pathway in MM
Cyt‑c↑, BA mediated the release of cyt c and activated cleaved caspase-3, caspase-8, and caspase-9 and cleaved PARP1
Casp3↑,
Casp8↑,
Casp9↑,
cl‑PARP1↑,
MDA↑, here is a concentration-dependent increase in MDA contents and reduction in SOD activities, especially for the high concentration group.
SOD↓,
SOD2↓, expression of genes SOD2, FHC, GCLM, and GSTM was all decreased following treatment with BA (40 μM)
GCLM↓,
GSTA1↓,
FTH1↓, FHC
GSTs↓, GSTM
TumVol↓, BA Inhibits the Growth of MM Xenograft Tumors In Vivo. BA-treated group were significantly reduced (inhibition ratio of approximately 72.1%).

2733-

BetA,

Betulinic Acid Inhibits Cell Proliferation in Human Oral Squamous Cell Carcinoma via Modulating ROS-Regulated p53 Signaling

in-vitro,

Oral,

12.5–100 μM BA for 24–72 h

in-vivo,

NA,

BA against OSCC in implanted mice in vivo

TumCP↓, BA dose-dependently inhibited KB cell proliferation and decreased implanted tumor volume.
TumVol↓,
mt-Apoptosis↑, BA significantly promoted mitochondrial apoptosis, as reflected by an increase in TUNEL+ cells and the activities of caspases 3 and 9, an increase in Bax expression, and a decrease in Bcl-2 expression and the mitochondrial oxygen consumption rate.
Casp3↑,
Casp9↑,
BAX↑,
Bcl-2↑,
OCR↓, BA dose-dependently decreased the oxygen consumption rate, indicating that BA induced a significant mitochondrial dysfunction
TumCCA↑, BA significantly increased cell population in the G0/G1 phase and decreases the S phase cell number, indicating the occurrence of G0/G1 cell cycle arrest.
ROS↑, ROS generation was significantly increased by BA
eff↓, and antioxidant NAC treatment markedly inhibited the effect of BA on apoptosis, cell cycle arrest, and proliferation.
P53↑, BA dose-dependently increased p53 expression in KB cells and implanted tumors.
STAT3↓, Inhibition of STAT3 Signaling Is Involved in BA-Induced Suppression of Cell Proliferation
cycD1/CCND1↑, We found that BA mainly increased the mRNA expression of cyclin D1 but had no significant effect on cyclin E, CDK2, CDK4, or CDK6 expression.

2746-

BetA,

Betulinic acid induces apoptosis and inhibits metastasis of human colorectal cancer cells in vitro and in vivo

in-vitro,

CRC,

HCT116

in-vivo,

CRC,

20 mg/kg/day of BA

TumCG↓, BA inhibited colorectal cancer cell lines in vitro with a time-dependent and dose-dependent manner.
BAX↑, upregulating expression of Bax and cleaved caspase-3 and downregulating protein of Bcl-2
Bcl-2↓,
ROS↑, BA could increase the production of reactive oxygen species and reduce mitochondrial membrane potential of cancer cell, suggesting that BA induced cancer cells apoptosis by mitochondrial mediated pathways
MMP↓,
TIMP2↑, BA significantly inhibited the migration and invasion of colorectal cancer cells, reduced the expression of matrix metalloproteinase (MMPs) and increased the expression of MMPs inhibitor (TIMP-2).
TumVol↓,

5692-

BJ,

Seed oil of Brucea javanica induces apoptosis through the PI3K/Akt signaling pathway in acute lymphocytic leukemia Jurkat cells

vitro+vivo,

AML,

Apoptosis↑, BJOE induced apoptosis in Jurkat cells and were suggestive of intrinsic apoptotic induction
Akt↓, BJOE inhibited Akt (protein kinase B) activation and upregulated its downstream targets p53 and FoxO1 (forkhead box gene, group O-1) to initiate apoptosis
P53↑,
FOXO1↑,
GSK‐3β↑, The activation of GSK3β was also involved.
TumVol↓, In a 96-case clinical trial, BJOE treatment reduced tumor size and improved the quality of life for patients with gastrointestinal cancer and cervical cancer [18].
QoL↑,
BBB↑, As shown in pharmacokinetic studies, BJOE crossed the blood-brain barrier
OS↑, In another 100-case clinical trial, BJOE prolonged the survival of patients with brain meta- stases from lung cancer [24].
Dose↝, Currently, BJOE is intravenously administered for the clinical treatment of lung cancer [25-28] and gastric cancer [29-31]
MMP↓, MMP collapse and ROS production in Jurkat cells were also observed following BJOE treatment.
ROS↑,
XIAP↑, we found that BJOE targeted Akt to stimulate FoxO1 and XIAP to induce apoptosis.
Casp9↑, BJOE promoted the activation of caspase- 9, caspase-8 and caspase-3.
Casp8↑,
Casp3↑,
cl‑PARP↑, The cleavage of PARP proteins was also observed.
TumCCA↑, the sub-G1 phase cell percentages increased in all five samples in a BJOE concentration-dependent manner.

5683-

BML,

Bromelain inhibits COX-2 expression by blocking the activation of MAPK regulated NF-kappa B against skin tumor-initiation triggering mitochondrial death pathway

in-vitro,

NA,

COX2↓, Bromelain inhibits COX-2 expression by blocking the activation of MAPK regulated NF-kappa B against skin tumor-initiation triggering mitochondrial death pathway
MAPK↓,
NF-kB↓,
TumMeta↓, Pre-treatment of bromelain resulted in reduction in cumulative number of tumors (CNT) and average number of tumors per mouse.
P53↑, Bromelain treatment resulted in upregulation of p53 and Bax and subsequent activation of caspase 3 and caspase 9 with concomitant decrease in Bcl-2.
BAX↑,
Casp3↑,
Casp9↑,
Bcl-2↓,
MAPK↓, bromelain treatment curtailed extracellular signal regulated protein kinase (ERK1/2), p38 mitogen-activated protein kinase (MAPK) and Akt activity
ERK↓,
Akt↓,
TumVol↓, ~33% inhibition in tumor volume

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↑,

3518-

Bor,

Boron Report

Review,

Var,

Review,

AD,

Risk↓, Boron reduces prostate cancer incidence by up to 64%
serineP↓, Boric acid acts to inhibit serine proteases—it decreases PSA by 87% and reduces tumor size in a prostate cancer mouse model
PSA↓,
TumVol↓,
IGF-1↓, expression of IGF-1 (insulin-like growth factor type 1) was markedly reduced by boron treatment. Circulating blood levels of IGF-1 were not reduced in the treated mice, however.
*Mag↑, In situations of adequate calcium supply but deficient magnesium resources, boron appears to substitute or “pinch hit” for magnesium during the process of bone formation.
*Calcium↑, The effect of boron on raising plasma calcium levels may, in part, be due to its enhancing effect on vitamin D.1
*VitD↑,
*COX2↓, boron has been shown to inhibit cyclooxygenase (COX) and lipoxygenase (LOX).
*5LO↓,
*PGE2↓, leads to a decrease in prostaglandin E2 (PGE2)
*NF-kB↓, suppressing nuclear factor kappa beta (NfkappaB)
*cognitive↑, Since it is now commonly accepted that the routine use of NSAIDs significantly reduces the incidence of Alzheimer’s disease,31,32 it is not surprising that papers have been published on boron’s positive effect on cognitive function.

696-

Bor,

Nothing Boring About Boron

Review,

Var,

>3mg

upper intake level (UL) of 20 mg/d

*hs-CRP↓, reduces levels of inflammatory biomarkers, such as high-sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor μ (TNF-μ);
*TNF-α↓,
*SOD↑, raises levels of antioxidant enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase
*Catalase↑,
*GPx↑,
*cognitive↑, improves the brains electrical activity, cognitive performance, and short-term memory for elders; restricted boron intake adversely affected brain function and cognitive performance.
*memory↑, In humans, boron deprivation (<0.3 mg/d) resulted in poorer performance on tasks of motor speed and dexterity, attention, and short-term memory.
*Risk↓, Boron-rich diets and regions where the soil and water are rich in boron correlate with lower risks of several types of cancer, including prostate, breast, cervical, and lung cancers.
*SAM-e↑,
*NAD↝, Boron strongly binds oxidized NAD+,76 and, thus, might influence reactions in which NAD+ is involved
*ATP↝,
*Ca+2↝, Because of its positive charge, magnesium stabilizes cell membranes, balances the actions of calcium, and functions as a signal transducer
HDAC↓, some boronated compounds are histone deacetylase inhibitors
TumVol↓,
IGF-1↓, expression of IGF-1 in the tumors was significantly reduced by boron treatment
PSA↓, Boronic acid has been shown to inhibit PSA activity.
Cyc↓, boric acid inhibits the growth of prostate-cancer cells both by decreasing expression of A-E cyclin
TumCMig↓,
*serineP↓, Boron exists in the human body mostly in the form of boric acid, a serine protease inhibitor.
HIF-1↓, shown to greatly inhibit hypoxia-inducible factor (HIF) 1
*ChemoSideEff↓, An in vitro study found that boric acid can help protect against genotoxicity and cytotoxicity that are induced in lymphocytes by paclitaxel
*VitD↑, greater production of 25-hydroxylase, and, thus, greater potential for vitamin-D activation
*Mag↑, Boron significantly improves magnesium absorption and deposition in bone
*eff↑, boron increases the biological half-life and bioavailability of E2 and vitamin D.
Risk↓, risk of prostate cancer was 52% lower in men whose diets supplied more than 1.8 mg/d of boron compared with those whose dietary boron intake was less than or equal to 0.9 mg/d.
*Inflam↓, As research into the chemistry of boron-containing compounds has increased, they have been shown to be potent antiosteoporotic, anti-inflammatory, and antineoplastic agents
*neuroP↑, In addition, boron has anti-inflammatory effects that can help alleviate arthritis and improve brain function and has demonstrated such significant anticancer
*Calcium↑, increase serum levels of estradiol and calcium absorption in peri- and postmenopausal women.
*BMD↑, boron stimulates bone growth in vitamin-D deficient animals and alleviates dysfunctions in mineral metabolism characteristic of vitamin-D deficiency
*chemoP↑, may help ameliorate the adverse effects of traditional chemotherapeutic agents. boric acid can help protect against genotoxicity and cytotoxicity that are induced in lymphocytes by paclitaxel, an anticancer drug commonly used to treat breast, ovarian
AntiCan↑, demonstrated preventive and therapeutic effects in a number of cancers, such as prostate, cervical, and lung cancers, and multiple and non-Hodgkin’s lymphoma
*Dose↑, only an upper intake level (UL) of 20 mg/d for individuals aged ≥ 18 y.
*Dose↝, substantial number of articles showing benefits support the consideration of boron supplementation of 3 mg/d for any individual who is consuming a diet lacking in fruits and vegetables
*BMPs↑, Boron was also found to increase mRNA expression of alkaline phosphatase and bone morphogenetic proteins (BMPs)
*testos↑, 1 week of boron supplementation of 6 mg/d, a further study by Naghii et al20 of healthy males (n = 8) found (1) a significant increase in free testosterone,
angioG↓, Inhibition of tumor-induced angiogenesis prevents growth of many types of solid tumors and provides a novel approach for cancer treatment; thus, HIF-1 is a target of antineoplastic therapy.
Apoptosis↑, Cancer cells, however, commonly overexpress sugar transporters and/or underexpress borate export, rendering sugar-borate esters as promising chemopreventive agents
*selectivity↑, In normal cells, the 2 latter, cell-destructive effects do not occur because the amount of borate present in a healthy diet, 1 to 10 mg/d, is easily exported from normal cells.
*chemoPv↑, promising chemopreventive agents

746-

Bor,

Organoboronic acids/esters as effective drug and prodrug candidates in cancer treatments: challenge and hope

Review,

NA,

50 mM CCL-233 colon

eff↑, newly developed boron-containing compounds have already demonstrated highly promising activities
*toxicity↓, Boronic acid/ester has been successfully incorporated into cancer treatments and therapy mainly due to its remarkable oxophilicity and low toxicity levels in the body
ROS↑, can trigger tumour microenvironmental abnormalities such as high levels of reactive oxygen species (ROS) and overexpressed enzymes
LAT↓, boron accumulation were observed to counterpart LAT-1 expression in a bone metastasis model of breast cancer
AntiCan↑, high concentration of boron in males reduces the probability of prostate cancer by 54% compared to males with low boron concentrations
AR↓, bortezomib
PSMB5↓, bortezomib
IGF-1↓, insulin-like growth factor 1 (IGF-1) in tumours was markedly reduced by boric acid.
PSA↓, exposure to both low-and high-dose boron supplementation, prostate-specific antigen (PSA) levels dropped by an average of 87%, while tumour size declined by an average of 31.5%
TumVol↓,
eff↑, phenylboronic acid is a more potent inhibitor than boric acid in targeting metastatic and proliferative properties of prostate cancer cells
Rho↓, RhoA, Rac1
Cdc42↓,
Ca+2↓, ER Ca+2 depletion occurred after the treatment of DU-145 prostate cancer cells with the physiological concentrations of boric acid
eff↑, boric acid (BA), sodium pentaborate pentahydrate (NaB), and sodium perborate tetrahydrate (SPT) against SCLC cell line using DMS-114 cells

706-

Bor,

Boron supplementation inhibits the growth and local expression of IGF-1 in human prostate adenocarcinoma (LNCaP) tumors in nude mice

in-vivo,

Pca,

LNCaP

1.7, mgB/kg/day

mice

TumVol↓, 38%
IGF-1↓, in tumors
PSA↓, 89%

4624-

Bor,

VitD3,

Boron as a Medicinal Ingredient in Oral Natural Health Products

Review,

Pca,

*Half-Life↝, (Boron) is excreted with a half-life of 21 hours, and is mostly eliminated with only a low level of accumulation in bone.
*eff↑, 13 subjects predetermined to be vitamin D deficient found that during a 60-day supplementation period with 6 mg boron/day, serum 25-hydroxyvitamin D levels rose by an average of 20%
PSA↓, one study using nude mice implanted with human prostate adenocarcinoma (LNCaP) cells found that boron supplementation reduced serum prostate-specific antigen (PSA) levels, and reduced tumor size and expression of IGF-1,
TumVol↓,
IGF-1↓,
*memory↓, Boron deprivation : results in significantly poorer performance on tasks involving eye-hand coordination, attention, and short-term memory (Penland 1994 and 1998).
*motorD↓,

1169-

Bos,

Boswellic Acid Inhibits Growth and Metastasis of Human Colorectal Cancer in Orthotopic Mouse Model By Downregulating Inflammatory, Proliferative, Invasive, and Angiogenic Biomarkers

in-vivo,

CRC,

50-200 mg/kg

mice

TumCG↓,
TumVol↓,
Weight∅, without significant decreases in body weight
ascitic↓,
TumMeta↓,
Ki-67↓,
CD31↓,
NF-kB↓,
COX2↓,
Bcl-2↓,
Bcl-xL↓,
IAP1↓,
survivin↓,
cycD1/CCND1↓,
ICAM-1↓,
MMP9↓,
CXCR4↓,
VEGF↓,

1230-

CA,

Caff,

Caffeine and Caffeic Acid Inhibit Growth and Modify Estrogen Receptor and Insulin-like Growth Factor I Receptor Levels in Human Breast Cancer

in-vitro,

BC,

MCF-7

in-vitro,

BC,

MDA-MB-231

Human,

NA,

cohort of 1,090 patients with invasive primary breast cancer in Sweden

TumVol↓, Moderate (2-4 cups/day) to high (≥5 cups/day) coffee intake was associated with smaller invasive primary tumors
TumCG↓,
ER(estro)↓,
cycD1/CCND1↓,
IGF-1R↓,
p‑Akt↓,

5749-

CA,

Rad,

Antitumor and Radiosensitizing Effects of Zinc Oxide-Caffeic Acid Nanoparticles against Solid Ehrlich Carcinoma in Female Mice

vitro+vivo,

BC,

MCF-7

Female Mice

NA,

Liver,

HepG2

RadioS↑, Combined treatment of ZnO-CA NPs with γ-irradiation improved these effects.
TumVol↓, ZnO-CA NPs resulted in a considerable decline in tumor size and weight, down-regulation of B-cell lymphoma 2 (BCL2) and nuclear factor kappa B (NF-κB) gene expressions, decreased vascular cell adhesion molecule 1 (VCAM-1) level
Bcl-2↓,
NF-kB↓,
VCAM-1↓,
ERK↓, ownregulation of phosphorylated-extracellular-regulated kinase 1 and 2 (p-ERK1/2) protein expression, DNA fragmentation and a recognizable peak at sub-G0/G1 indicating dead cells’ population in cancer tissues.
DNAdam↑,
TumCCA↑,

2013-

CAP,

Capsaicin, a component of red peppers, inhibits the growth of androgen-independent, p53 mutant prostate cancer cells

in-vitro,

Pca,

PC3

0-5 x 10-4 mol/L

in-vitro,

Pca,

LNCaP

in-vitro,

Pca,

DU145

in-vivo,

NA,

5 mg/kg/d;

mice

TumCP↓, profound antiproliferative effect on prostate cancer cells, inducing the apoptosis of both androgen receptor (AR)-positive (LNCaP) and -negative (PC-3, DU-145) prostate cancer cell lines
P53↑, increase of p53, p21, and Bax
P21↑,
BAX↑,
PSA↓, Capsaicin down-regulated the expression of not only prostate-specific antigen (PSA) but also AR
AR↓,
NF-kB↓, Capsaicin inhibited NF-kappa activation by preventing its nuclear migration
Proteasome↓, capsaicin inhibits proteasome activity which suppressed the degradation of IkappaBalpha
TumVol↓, Capsaicin, when given orally, significantly slowed the growth of PC-3 prostate cancer xenografts
eff∅, However, our experiments using the three TRVP1-inhibitors capsazepine, ruthenium red, and SB366791, did not show any attenuation of the inhibitory activity of capsaicin.

5886-

CAR,

Inhibition of TRPM7 with carvacrol suppresses glioblastoma functions in vivo

in-vivo,

GBM,

U87MG

flank xenograft GBM mouse model

in-vivo,

GBM,

U251

TRPM7↓, TRPM7 inhibitor, carvacrol
TumVol↓, carvacrol significantly reduced the tumour size in both mice injected with U87 and U251 cells, decreased p-Akt protein level and increased p-GSK3β protein levels
p‑Akt↓,
p‑GSK‐3β↑,
Dose↝, The carvacrol group received intraperitoneal injections (20, 40, or 60 mg/kg/day) for 5 days.

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↓,

1106-

CGA,

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

vitro+vivo,

BC,

MCF-7

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

6001-

Chit,

Recent advances in engineering chitosan-based nanoplatforms in biotherapeutic multi-delivery for multi-targeted disease treatments: Promises and outlooks

Review,

Var,

HepG2

Review,

AD,

TumVol↓, chitosan-based nanoparticles reduced tumors (doxorubicin (DOX) + survivin siRNA and curcumin + siRNA).
toxicity↓, Their initial studies reveal low toxicity and long-term medication delivery.
Half-Life↑,
eff↑, that allows drug release in reductive cellular environments (especially cancer cells with elevated glutathione levels),
selectivity↑, This clever nanocarrier reacts to intracellular cues and delivers its therapeutic payload mostly to cancer cells while protecting healthy tissues
Dose↝, These co-delivery systems take advantage of chitosan's mucoadhesive properties and protection against enzymatic degradation, enabling oral or nasal administration routes that traditionally pose challenges for peptide delivery
*BDNF↑, Chitosan nanoparticles delivering a combination of brain-derived neurotrophic factor (BDNF) protein and Nrf2 plasmid DNA have been shown to support synaptic plasticity, inhibit oxidative stress, and slow neurodegeneration.
*NRF2↑,
*ROS↓,
*neuroP↑,
*memory↑, In preclinical trials, such strategies improved memory retention, cognitive performance, and neuronal survival in rodent models
*cognitive↑,
*Obesity↓, obese non-human primates illustrated how chitosan-based codelivery of metformin and fibroblast growth factor 21 (FGF21) plasmid DNA targeted adipose tissue to achieve a 40 % reduction in visceral fat

2784-

CHr,

Chrysin targets aberrant molecular signatures and pathways in carcinogenesis (Review)

Review,

Var,

Apoptosis↑, apoptosis, disrupting the cell cycle and inhibiting migration without generating toxicity or undesired side‑effects in normal cells
TumCMig↓,
*toxicity↝, toxic at higher doses and the recommended dose for chrysin is <3 g/day
ChemoSen↑, chrysin also inhibits multi‑drug resistant proteins and is effective in combination therapy
*BioAv↓, extremely low bioavailability in humans due to rapid quick metabolism, removal and restricted assimilation. The bioavailability of chrysin when taken orally has been estimated to be between 0.003 to 0.02%
Dose↝, safe and effective in various studies where volunteers have taken oral doses ranging from 300 to 625 mg without experiencing any documented effect
neuroP↑, Chrysin has been shown to exert neuroprotective effects via a variety of mechanisms, such as gamma-aminobutyric acid mimetic properties, monoamine oxidase inhibition, antioxidant, anti-inflammatory and anti-apoptotic activities
*P450↓, Chrysin inhibits cytochrome P450 2E1, alcohol dehydrogenase and xanthine oxidase at various dosages (20 and 40 mg/kg body weight) and protects Wistar rats against oxidative stress
*ROS↓,
*HDL↑, ncreased the levels of high-density lipoprotein cholesterol, glutathione S-transferase, superoxide dismutase and catalase
*GSTs↑,
*SOD↑,
*Catalase↑,
*MAPK↓, inactivate the MAPK/JNK pathway and suppress the NF-κB pathways, and at the same time upregulate the expression of PTEN, and activate the VEGF/AKT pathway
*NF-kB↓,
*PTEN↑,
*VEGF↑,
ROS↑, chrysin treatment in ovarian cancer led to the augmented generation of reactive oxygen species, a decrease in MMP and an increase in cytoplasmic Ca2+,
MMP↓,
Ca+2↑,
selectivity↑, It has been found that chrysin has no cytotoxic effect on normal cells, such as fibroblasts
PCNA↓, Chrysin likewise downregulates proliferating cell nuclear antigen (PCNA) expression in cervical carcinoma cells
Twist↓, Chrysin decreases the expression of TWIST 1 and NF-κB and thus suppresses epithelial-mesenchymal transition (EMT) in HeLa cells
EMT↓,
CDKN1C↑, Chrysin administration led to the upregulation of CDKN1 at the transcript and protein leve
p‑STAT3↑, Chrysin decreased the viability of 4T1 breast cancer cells by suppressing hypoxia-induced phosphorylation of STAT3
MMP2↓, chrysin-loaded PGLA/PEG nanoparticles modulated TIMPS and MMP2 and 9, and PI3K expression in a mouse 4T1 breast tumor model
MMP9↓,
eff↑, Chrysin used alone and as an adjuvant with metformin has been found to downregulate cyclin D and hTERT expression in the breast cancer cell line
cycD1/CCND1↓,
hTERT/TERT↓,
CLDN1↓, CLDN1 and CLDN11 expression have been found to be higher in human lung squamous cell carcinoma. Treatment with chrysin treatment reduces both the mRNA and protein expression of these claudin genes
TumVol↓, Treatment with chrysin treatment (1.3 mg/kg body weight) significantly decreases tumor volume, resulting in a 52.6% increase in mouse survival
OS↑,
COX2↓, Chrysin restores the cellular equilibrium of cells subjected to benzopyrene by downregulating the expression of elevated proteins, such as PCNA, NF-κB and COX-2
eff↑, quercetin and chrysin together decreased the levels of pro-inflammatory molecules, such as IL-6, -1 and -10, and the levels of TNF via the NF-κB pathway.
CDK2↓, Chrysin has been shown to inhibit squamous cell carcinoma via the modulation of Rb and by decreasing the expression of CDK2 and CDK4
CDK4↓,
selectivity↑, chrysin selectively exhibits toxicity and induces the self-programed death of human uveal melanoma cells (M17 and SP6.5) without having any effect on normal cells
TumCCA↑, halting the cell cycle at the G2/M or G1/S phases
E-cadherin↑, upregulation of E-cadherin and the downregulation of cadherin
HK2↓, Chrysin decreased expression of HK-2 in mitochondria, and the interaction between HK-2 and VDAC 2 was disrupted,
HDAC↓, Chrysin, a HDAC inhibitor, caused cytotoxicity, and also inhibited migration and invasion.

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↑,

Showing Research Papers: 1 to 50 of 134
Page 1 of 3 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 134

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

Bacteria↓, 1,
Total Targets: 216

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Catalase↑, 2, GPx↑, 1, GSTs↑, 1, HDL↑, 1, NRF2↑, 1, ROS↓, 2, SAM-e↑, 1, SOD↑, 2,

Mitochondria & Bioenergetics ⓘ

ATP↝, 1,

Core Metabolism/Glycolysis ⓘ

NAD↝, 1,

Cell Death ⓘ

MAPK↓, 1,

Proliferation, Differentiation & Cell State ⓘ

PTEN↑, 1,

Migration ⓘ

5LO↓, 1, Ca+2↝, 1, serineP↓, 1,

Angiogenesis & Vasculature ⓘ

VEGF↑, 1,

Immune & Inflammatory Signaling ⓘ

COX2↓, 1, Inflam↓, 1, NF-kB↓, 2, PGE2↓, 1, TNF-α↓, 1, VitD↑, 2,

Synaptic & Neurotransmission ⓘ

BDNF↑, 1,

Hormonal & Nuclear Receptors ⓘ

testos↑, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 1, Dose↑, 1, Dose↝, 1, eff↑, 2, Half-Life↝, 1, P450↓, 1, selectivity↑, 1,

Clinical Biomarkers ⓘ

BMD↑, 1, BMPs↑, 1, Calcium↑, 2, hs-CRP↓, 1, Mag↑, 2, VitD↑, 2,

Functional Outcomes ⓘ

chemoP↑, 1, chemoPv↑, 1, ChemoSideEff↓, 1, cognitive↑, 3, memory↓, 1, memory↑, 2, motorD↓, 1, neuroP↑, 2, Obesity↓, 1, Risk↓, 1, toxicity↓, 2, toxicity↝, 3,
Total Targets: 49

Scientific Paper Hit Count for: TumVol, Tumor Volume

15 Magnetic Fields
9 Silver-NanoParticles
7 Curcumin
7 Quercetin
7 Magnetic Field Rotating
6 doxorubicin
5 Apigenin (mainly Parsley)
5 Boron
4 EGCG (Epigallocatechin Gallate)
4 Shikonin
4 Thymoquinone
3 Vitamin C (Ascorbic Acid)
3 Ashwagandha(Withaferin A)
3 Betulinic acid
3 Hydrogen Gas
3 immunotherapy
3 metronomic chemo
3 Silymarin (Milk Thistle) silibinin
2 Photodynamic Therapy
2 Gold NanoParticles
2 Allicin (mainly Garlic)
2 Baicalein
2 Berberine
2 Caffeic acid
2 Radiotherapy/Radiation
2 Cisplatin
2 Dichloroacetate
2 Orlistat
2 Honokiol
2 capecitabine
2 Naringin
2 Aflavin-3,3′-digallate
1 3-bromopyruvate
1 cetuximab
1 chemodynamic therapy
1 EMF
1 wortmannin
1 Ajoene (compound of Garlic)
1 Alpha-Lipoic-Acid
1 low dose naltrexone
1 Artemisinin
1 Berbamine
1 Brucea javanica
1 Bromelain
1 borneol
1 Vitamin D3
1 Boswellia (frankincense)
1 Caffeine
1 Zinc
1 Capsaicin
1 Carvacrol
1 Cannabidiol
1 Celastrol
1 Chlorogenic acid
1 chitosan
1 Chrysin
1 Oxaliplatin
1 Metformin
1 Bortezomib
1 diet FMD Fasting Mimicking Diet
1 Chemotherapy
1 diet Methionine-Restricted Diet
1 Evodiamine
1 Docetaxel
1 Electrical Pulses
1 Fucoidan
1 Ferulic acid
1 Fenbendazole
1 Gallic acid
1 Garcinol
1 Graviola
1 HydroxyCitric Acid
1 Hyperthermia
1 Licorice
1 Lycopene
1 Melatonin
1 Bicarbonate(Sodium)
1 Phenylbutyrate
1 Piperine
1 probiotics
1 Pterostilbene
1 enzalutamide
1 Resveratrol
1 Rutin
1 salinomycin
1 Selenium
1 Oxygen, Hyperbaric
1 Sulforaphane (mainly Broccoli)
1 Iron
1 Salvia miltiorrhiza
1 Thymol-Thymus vulgaris
1 Magnesium
1 Vitamin K2
1 Xylitol
1 Zerumbone
1 5-fluorouracil

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#:530  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

TumVol Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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