TumCP Cancer Research Results

TumCP, Tumor Cell proliferation: Click to Expand ⟱

Source:

Type:

Tumor cell proliferation is a key characteristic of cancer. It refers to the rapid and uncontrolled growth of cells that can lead to the formation of tumors.

Scientific Papers found: Click to Expand⟱

1123-

aLinA,

Linoleic acid induces an EMT-like process in mammary epithelial cells MCF10A

in-vitro,

BC,

LA is cancer promoting

in-vitro,

NA,

MCF10

TumCP↑, Linoleic acid (LA) induces proliferation and invasion in breast cancer cells.
E-cadherin↓,
Snail↑, increase of Snail1, Snail2, Twist1, Twist2 and Sip1 expressions.
Twist↑,
ZEB2↑,
FAK↑,
NF-kB↑,
MMP2↓, Furthermore, LA induces FAK and NFκB activation, MMP-2 and -9 secretions, migration and invasion.
MMP9↓,
*EMT↑, LA promotes an EMT-like process in MCF10A
TumCI↑,

5380-

ART/DHA,

Artemisinin and Its Derivatives as Potential Anticancer Agents

Review,

Var,

TumCG↓, Artemisinin (1, Figure 2) could suppress cell growth [16], reduce angiogenesis-related factors [17], and induce ferroptosis [18] in breast cancer cell lines
angioG↓,
Ferroptosis↑,
TumCP↑, Dihydroartemisinin (2, Figure 2) exhibited anticancer effects against breast cancer by suppressing cell proliferation [16], inhibiting angiogenesis [19], inducing autophagy [20] and pyroptosis [21], and targeting cancer stem cells (CSCs) [
TumAuto↑,
CSCs↑,
eff↑, Dihydroartemisinin is more potent than artemisinin, as the IC50 values at 24 h were lower on MCF-7 (129.1 μM versus 396.6 μM) and MDA-MB-231 (62.95 μM versus 336.63 μM)
YAP/TEAD↓, Additionally, dihydroartemisinin was proven to have the ability to reduce the expression of yes-associated protein 1 (YAP1), which has been commonly used as a prognostic marker in liver cancer.
TumCCA↑, induced G0/G1 cell cycle arrest and apoptosis by promoting oxygen species (ROS) accumulation.
ROS↑,
ChemoSen↑, The application of combination treatment using artemisinin and its derivatives with commonly used chemotherapy drugs, such as cisplatin, carboplatin, doxorubicin, temozolomide, etc., always exhibits significantly improved anticancer effects
N-cadherin↓, and inhibiting the proliferation, colony formation, and invasiveness of colon cancer cells by inhibiting NRP2, N-cadherin, and Vimentin expression
Vim↓,
MMP9↓, by decreasing the expression of HuR and matrix metalloproteinase (MMP)-9 proteins [24],
eff↑, Further investigations suggested that both dihydroartemisinin treatment and the loss of PRIM2 could lead to a decreased GSH level and induce cellular lipid ROS and mitochondrial MDA expression.
STAT3↓, Recently, artemisinin and its derivatives were reported to have potential as direct STAT3 inhibitors [98].
CD133↓, dihydroartemisinin treatment could significantly reduce the expression of CSC markers (CD133, CD44, Nanog, c-Myc, and OCT4) by downregulating Akt/mTOR pathway
CD44↓,
Nanog↓,
cMyc↓,
OCT4↓,
Akt↓,
mTOR↓,

4804-

ASTX,

Astaxanthin in cancer therapy and prevention (Review)

Review,

Var,

Review,

AD,

*antiOx↑, gained significant attention for its potent antioxidant, anti-inflammatory and anti-proliferative properties.
*Inflam↓,
ChemoSen⇅, In some instances, it reduces the cytotoxicity of cisplatin, particularly with cisplatin on the SKBR3 breast cancer cell line, indicating a potential protective effect. In certain cases, AXT enhances the cytotoxic effect of the chemotherapy drugs
chemoP↑, The present review detailed both in vitro and in vivo studies highlighting the effectiveness of AXT in sensitizing cancer cells to chemotherapy, thereby enhancing therapeutic outcomes and potentially reducing treatment-related side effects.
BioAv↑, incorporation of AXT in nanoparticle-based delivery systems has further improved its bioavailability
TumCP↑, AXT exhibits hormetic effects on U251-MG, T98G and CRT-MG cell lines, where low doses stimulate cell proliferation
ROS⇅, while higher doses induce apoptosis by triggering a dose-dependent oxidative stress response, significantly increasing reactive oxygen species (ROS) levels and promoting apoptosis
Apoptosis↑,
PI3K↑, AXT activates the PI3K/Akt/GSK3β pathway, leading to the upregulation of nuclear factor erythroid 2-related factor 2 (Nrf2), a transcription factor, in SH-SY5Y cells under oxygen and glucose deprivation conditions
Akt↑,
GSK‐3β↑,
NRF2↑,
AntiCan↑, antioxidant, AXT has the potential to act as both an anticancer drug and a neuroprotectant.
*neuroP↑, AXT protects against oxidative stress, which causes mitochondrial dysfunction and apoptosis, thereby reducing the detrimental effects associated with neurodegenerative diseases such as Alzheimer's, Parkinson's
eff↑, The synergistic cytotoxic effect of AXT with melatonin showed enhanced efficacy in the T47D cell line compared with the MDA-MB-231 line
AntiTum↑, AXT effectively reduced tumor size and the number of cancer cells in mice, supporting its potential anti-tumor activity.

1385-

BBR,

5-FU,

Low-Dose Berberine Attenuates the Anti-Breast Cancer Activity of Chemotherapeutic Agents via Induction of Autophagy and Antioxidation

in-vitro,

BC,

MCF7

BBR (0-10 μM) with 5-FU (0-250 μM)

in-vitro,

BC,

MDA-MB-231

eff↓, Berberine Attenuates the Anti-Breast Cancer Activity of Chemotherapeutic Agents
ROS↑, LDB mildly while HDB greatly stimulated ROS generation BBR-induced ROS generation may activate the antioxidant response therefore to promote cancer cell proliferation.
TumCP↑,
NRF2↑,
ChemoSen↓, These findings revealed a potential negative impact of BBR on its adjuvant anti-breast cancer therapy

5178-

BBR,

Berberine, a natural product, induces G1-phase cell cycle arrest and caspase-3-dependent apoptosis in human prostate carcinoma cells

in-vitro,

Pca,

DU145

in-vitro,

Pca,

PC3

TumCP↑, Here, we report that in vitro treatment of androgen-insensitive (DU145 and PC-3) and androgen-sensitive (LNCaP) prostate cancer cells with berberine inhibited cell proliferation and induced cell death in a dose-dependent (10–100 μmol/L) and time-depe
TumCCA↑, associated with G1-phase arrest, which in DU145 cells was associated with inhibition of expression of cyclins D1, D2, and E and cyclin-dependent kinase (Cdk) 2, Cdk4, and Cdk6 proteins,
cycD1/CCND1↓,
cycE/CCNE↓,
CDK2↓,
CDK4↓,
CDK6↓,
P21↑, increased expression of the Cdk inhibitory proteins (Cip1/p21 and Kip1/p27), and enhanced binding of Cdk inhibitors to Cdk.
p27↑,
Apoptosis↑, Berberine also significantly (P < 0.05–0.001) enhanced apoptosis of DU145 and LNCaP cells with induction of a higher ratio of Bax/Bcl-2 proteins
Bax:Bcl2↑,
MMP↓, disruption of mitochondrial membrane potential, and activation of caspase-9, caspase-3, and poly(ADP-ribose) polymerase.
Casp9↑,
Casp3↑,
PARP↑,
DNAdam↑, analysis of DNA fragmentation
selectivity↑, Berberine Inhibits Proliferation and Viability and Induces the Death of Prostate Cancer Cells but not of Normal Prostate Epithelial Cells
Cyt‑c↑, Berberine Induces the Disruption of Mitochondrial Membrane Potential and Increases the Release of Cytochrome c

6503-

BCP,

The Potential Therapeutic Role of Beta-Caryophyllene as a Chemosensitizer and an Inhibitor of Angiogenesis in Cancer

Review,

Var,

ChemoSen↑, Beta-Caryophyllene (BCP), was highlighted in several recent preclinical studies to enhance chemo-sensitization in chemo-resistant tumors and to efficiently inhibit angiogenesis and cancer cells’ ability to invade and metastasize.
angioG↓,
TumCI↓,
TumMeta↓,
ROS↑, BCP seems to work as a dual modulator of oxidative stress, increasing reactive oxygen species (ROS) in cancer cells, and thus enhancing apoptosis, but reducing ROS in normal cells to protect them from damage
*ROS↓,
chemoP↑,
CB2 / CNR2↑, important issue in BCP is its ability to bind to the body’s cannabinoid receptor 2 (CB2), where it binds selectively to the CB2 receptors and not the CB1 receptor, which makes it non-psychoactive and therapeutically appealing.
Inflam↓, activation of the CB2 receptor by BCP can suppress pro-inflammatory cytokines production, helping to create an anti-tumor immune environment
AntiTum↑,
*BioAv↑, Beta-Caryophyllene, a food additive approved by the Food and Drug Administration, is efficiently absorbed in the gastro-intestinal tract and can penetrate the blood–brain barrier and has a well-established safety profile, making it an attractive biom
*BBB↑,
Apoptosis↑, Induces apoptosis and suppresses proliferative activity of lung cancer cells
TumCP↑,
TumCCA↑, Induces G1 cell cycle arrest by dysregulating cyclins and other molecules
RadioS↑, GBM: Works as a potential radiosensitizer for improving RT outcomes by inhibiting DNA repair, inducing apoptosis, and suppressing anti-apoptotic and survival pathways
DNArepair↓,
ROS↑, BC: Enhances sensitization and promotes the cigarette smoke condensate (CSC)-induced apoptosis in MDA-MB-468 cells, mainly by triggering oxidative stress and inhibition of STAT3
STAT3↓,
*BioEnh↑, BCP is considered a key component in black pepper’s ability to enhance nutrient absorption, including compounds like curcumin.
Pain↓, BCP in cloves further supports their role in pain management and infection prevention.
AntiBio↓,
ROS↑, selectively induce apoptosis and oxidative stress in cancer cells while sparing normal cells at lower concentrations.
Dose↝, I50, for many cancer cell lines typically ranges from 19 to 64 μM
NF-kB↓, Beta-Caryophyllene was reported to inhibit the central to the regulators of inflammation, NF-κB and MAPK pathways, leading to a decrease in pro-inflammatory cytokine (TNF-α, IL-1β, and IL-6) production
MAPK↓,
TNF-α↓,
IL1β↓,
IL6↓,
cl‑PARP↑, through increasing the levels of cleaved PARP, caspases and Bax, and the downregulation of Bcl-2, directly by interaction with CB2.
Casp↑,
BAX↑,
Bcl-2↓,
VEGF↓, BCP blocks migration of endothelial cells by inhibiting the secretion of VEGF, and thus blocking the activity of the tyrosine kinase VEGFR2
VEGFR2↓,
MMP2↓, BCP can also prohibit the secretion of MMP-2, p-p38 and p-ERK
p‑p38↓,
p‑ERK↓,
EPR↑, BCP was suggested to accumulate in the cancer cell membrane, altering the cells’ permeability, leading to the accumulation of anticancer drugs, and consequently strengthening the drugs’ activity.
P-gp↓, direct inhibition of P-glycoprotein (P-gp/ABCB1) and multidrug resistance-associated protein 1 (MRP1/ABCC1), which are overexpressed in resistant tumors
MRP1/ABCC1↓,
*NRF2↑, Importantly, BCP’s selective antioxidant activity—activating Nrf2 in normal cells while increasing ROS in cancer cells—minimizes off-target toxicity,
*antiOx↑,

5842-

CAP,

Capsaicin: Current Understanding of Its Mechanisms and Therapy of Pain and Other Pre-Clinical and Clinical Uses

Review,

Nor,

Review,

Diabetic,

*Pain↓, capsaicin promotes pain relief when used in the right dosage and frequency.
*TRPV1↑, capsaicin-induced pain is also used to assess new molecules that target TRPV1 receptor. Capsaicin activates TRPV1
AMPK↑, The inhibitory effect of capsaicin on this process seems to involve the activation of 5’ adenosine monophosphate-activated protein kinase (AMPK) in conjunction with intracellular ROS release
ROS↑,
TumCP↑, AMPK activation is also linked to inhibition of cell proliferation and apoptosis [153,154]
Apoptosis↑,
TumCCA↑, capsaicin targets preadipocyte proliferation by blocking the S-phase of the cell cycle [149].
Casp3↑, capsaicin induces apoptosis in preadipocytes via the activation of caspase-3, Bax, and Bak, cleavage of PARP, and down-regulation of Bcl-2
BAX↑,
Bak↑,
cl‑PARP↑,
Bcl-2↓,
RNS↑, capsaicin induces apoptosis in BMSC via increased production of ROS and reactive nitrogen species (RNS) [
*glucose↓, healthy male volunteers revealed that capsaicin lowers glucose and increases insulin levels shortly after oral administration
*Insulin↑,
*BP↓, Capsaicin stimulates the release of CGRP through the activation of TRPV1 and therefore decreases blood pressure
*AntiAg↑, Capsaicin has been shown to inhibit platelet aggregation [199,200], which may also provide protection against cardiovascular diseases
ER Stress↑, endoplasmic reticulum stress in human nasopharyngeal carcinoma and pancreatic cancer cells,
Hif1a↓, capsaicin increases the degradation of hypoxia inducible factor 1α in non-small cell lung cancer,
chemoPv↑, mounting evidence supporting a chemo-preventive role for capsaicin in cancer cell culture and animal models,

1518-

CAP,

Capsaicin-mediated tNOX (ENOX2) up-regulation enhances cell proliferation and migration in vitro and in vivo

in-vitro,

CRC,

HCT116

ENOX2↑, low concentrations s (<10uM) of capsaicin up-regulates tNOX
TumCP↑,
TumCMig↑,
Dose?, <10uM
eff↑, tNOX knockdown reverses capsaicin-induced cell migration and growth

6182-

Cu,

Role of cuproptosis in digestive system tumors (Review)

Review,

Var,

Cupro↑, As copper dysregulation is common in cancer cells, targeting copper levels or metabolic pathways can trigger cuproptosis, thereby inhibiting tumor growth and progression.
TumCG↓,
Apoptosis↑, Copper can trigger multiple forms of cell death, including apoptosis, oxidative stress-induced necrosis, autophagy and ferroptosis
ROS↑,
Ferroptosis↑,
ETC↓, . Their disruption impairs the electron transport chain and decreases ATP synthesis and mitochondrial membrane potential (76).
MMP↓,
Ca+2↑, Consequently, mitochondrial energy production decreases, accompanied by increased inner membrane permeability, elevated Ca2+ concentration and the accumulation of ROS (77).
Fenton↑, Cu2+ catalyzes the Fenton-like reaction, generating hydroxyl radicals that initiate oxidative stress, leading to extensive cell damage and death (96)
lipid-P↑, These radicals also induce lipid peroxidation, compromising the integrity and fluidity of cell membranes and increasing membrane permeability (99).
MPT↑,
ATP↓, Excess ROS decrease the mitochondrial membrane potential and ATP synthesis and promote cytochrome c release, ultimately activating caspase cascades and triggering apoptosis
Cyt‑c↑,
Casp↑,
angioG↑, Mechanistically, copper promotes tumor progression through multiple pathways. First, copper stimulates angiogenesis by activating angiogenic factors and enhancing the proliferation and migration of vascular endothelial cells
TumCP↑,
TumCMig↑,
TumCI↑, Second, copper serves as a cofactor for several metalloenzymes, including MMP-9, SOD1, vascular adhesion protein-1 and lysyl oxidase (LOX), all of which are key for cancer invasion and metastasis
TumMeta↑,
DDS↑, tussah silk fibroin (TSF)-based nanoparticles (NPs) use TME-responsive release mechanisms to deliver copper and the cuproptosis-inducing drug ES directly to pancreatic cancer cells.
eff↑, suppressed by the copper chelator TTM, further confirming the mechanism of copper-induced cell death. Furthermore, 2-deoxy-D-glucose, a glycolysis inhibitor, can significantly enhance cuproptosis

1850-

dietFMD,

Fasting-mimicking diet remodels gut microbiota and suppresses colorectal cancer progression

in-vivo,

CRC,

mice

TumCP↑, FMD cycles effectively suppressed colorectal cancer growth, reduced cell proliferation and angiogenesis, increased tumor-infiltration lymphocytes especially CD8+T cells
angioG↓,
CD8+↑,
GutMicro↑, FMD stimulated protective gut microbiota, especially Lactobacillus.
eff↑, Additionally, FMD synthesizing with anti-PD-1 therapy effectively inhibited CRC progression.

5006-

DSF,

Cu,

Disulfiram targeting lymphoid malignant cell lines via ROS-JNK activation as well as Nrf2 and NF-kB pathway inhibition

vitro+vivo,

lymphoma,

TumCD↑, n combination with a low concentration (1 μM) of Cu2+, DS induced cytotoxicity in Raji cells with an IC50 of 0.085 ± 0.015 μM and in Molt4 cells with an IC50 of 0.435 ± 0.109 μM.
TumCP↑, DS/Cu inhibits the proliferation of Raji cells in vivo.
Apoptosis↑, After exposure to DS (3.3 μM)/Cu (1 μM) for 24 hours, apoptosis was detected in 81.03 ± 7.91% of Raji cells
NRF2↓, After 24 h exposure, DS/Cu inhibits Nrf2 expression.
ROS↑, DS/Cu induced ROS generation.
p‑JNK↑, DS/Cu induced phosphorylation of JNK and inhibits p65 expression as well as Nrf2 expression both in vitro and in vivo.
p65↓,
eff↓, N-acetyl-L-cysteine (NAC), an antioxidant, can partially attenuate DS/Cu complex-induced apoptosis and block JNK activation in vitro.
NF-kB↓, Moreover, ROS-related activation of JNK pathway and inhibition of NF-κB and Nrf2 may also contribute to the DS/Cu induced apoptosis.

6611-

Ech,

Proliferative activity of a blend of Echinacea angustifolia and Echinacea purpurea root extracts in human vein epithelial, HeLa, and QBC-939 cell lines, but not in Beas-2b cell lines

in-vitro,

Cerv,

HeLa

in-vitro,

Nor,

BEAS-2B

in-vitro,

Nor,

HUVECs

Imm↑, Echinacea is used for its immunostimulating properties and may have a role in modulating adverse immune effects of chemotherapy
TumCP↑, results of this study show that the hydroethanolic extract of Echinacea herbal medicine promotes the growth of HeLa cells and QBC-939 cancer cell proliferation, and may interfere with cancer treatment (i.e., chemotherapy drugs such as 5-fluorouracil
Telomerase↓, due to the major phytochemical chicoric acid (main constituent in Fig. 1) that reduces telomerase activity; induction of apoptosis via DNA fragmentation, activation of caspase-9, cleavage of PARP, and downregulation of β-catenin
Apoptosis↑,
DNAdam↑,
Casp9↑,
cl‑PARP↑,
β-catenin/ZEB1↓,

25-

EGCG,

QC,

Quercetin Increased the Antiproliferative Activity of Green Tea Polyphenol (-)-Epigallocatechin Gallate in Prostate Cancer Cells

in-vitro,

Pca,

PC3

 5, 10, 20 uM

in-vitro,

Pca,

LNCaP

 5, 10, 20 uM

COMT↓, fact that EGCG primarily inhibited COMT activity, whereas quercetin reduced the amount of COMT protein.
TumCP↑, Quercetin and EGCG in combination synergistically inhibited cell proliferation, caused cell cycle arrest, and induced apoptosis in PC-3 cells.
TumCCA↑,
Apoptosis↑,

6823-

EMD,

Role of emodin to prevent gastrointestinal cancers: recent trends and future prospective

Review,

Var,

AntiCan↑, Emodin (1,3,8-trihydroxy-6-methylanthraquinone), a natural compound derived from traditional Chinese and Japanese medicine, has recently garnered significant attention for its potential anticancer properties.
*antiOx↑, Emodin exerts its chemoprotective effects through a combination of antioxidative, anti-inflammatory, and anti-proliferative mechanisms.
*chemoP↑,
*Inflam↓,
TumCP↓,
TumMeta↓, emodin inhibits cancer metastasis, disrupts cell cycle progression, and impairs cancer cell survival.
TumCCA↑,
MAPK↑, activation of the p38 MAPK/JNK1/2 signaling pathway, the upregulation of pro-apoptotic factors such as Bax/Bcl-2 and caspases, and the enhancement of reactive oxygen species (ROS) levels (
BAX↑,
Casp↑,
ROS↑,
*BioAv↓, The pharmacokinetic limited properties of emodin significantly affect its bioavailability and bioactivity, hence limiting its therapeutic uses.
other↝, Chinese medicinal herbs contains emodin, which is utilized in traditional Chinese and Japanese medicine, include Rheum palmatum, Polygonum cuspidatum, and Cassia obtusifolia
TumCI↓, including as invasion and metastasis, tumour angiogenesis, epithelial-mesenchymal transition (EMT), cell growth (i.e., promotion of apoptosis, reduction of proliferation, and changed cellular redox status).
EMT↓,
TumCG↑,
Apoptosis↑,
TumCP↑,
MMP2↓, inhibit cell invasion by modulating and down regulating the activation and expression of MMP2, Bax/Bcl-2 and caspase-3 involving in esophageal cancer
Casp3↑,
ChemoSen↑, When combined with ciplatin, emodin significantly raises intracellular ROS, which improves proapoptotic effects and can be used to treat esophageal cancer
PI3K↓, figure 3
Akt↓,
Cyt‑c↑,
cl‑PARP↑,
MMP↓, emodin trigger the mitochondria of GI cancer cells to disrupt mitochondrial membrane potential by signaling molecules Bax, Bak PARP and triggers the release of cytochrome c to activate caspase -9 and 3 culminating into apoptosis
Warburg↓, Hepatic carcinoma HepG2 cells 20–200 µM Reduces wadburg effect by ↓ HKII, PKM2, LDHA, limiting energy supply, ↑ ROS production, ↑ mitochondrial damage and apoptosis
HK2↓,
PKM2↓,
LDHA↓,
mtDam↑,
Apoptosis↑,
N-cadherin↓, Ovarian cancer SK-OV-3, A2780, PA-1 2.5–80 µM Inhibited EMT by ↓ N cadherin & vimentin and ↑ E-cadherin
Vim↓,
E-cadherin↑,
eff↑, EMO exhibits broader range of pharmacological activities and in combination with nano range molecules.
eff↑, chitosan oligosaccharide nano-micelles (CSO-SA-EMO) significantly enhanced antioncogenic properties against the gastric cancer cells.
eff↑, Fe3O4- PEG-Cy7-EMO nanoparticles also proved potential nanoplatform in pancreatic tumor xenografted mice.
toxicity↝, emodin treatment at a maximum dose of 80 mg/Kg body weight orally and 40 mg/Kg body weight intraperitoneally does not significantly harm patients.
toxicity↑, emodin dosage higher than 500–1500 mg/Kg of body weight may cause toxicity such as hepatotoxicity and inflammation

2082-

HNK,

Revealing the role of honokiol in human glioma cells by RNA-seq analysis

in-vitro,

GBM,

U87MG

36.27 μM

In U87-MG cells, the optimum concentration of honokiol was 20 µM, and the optimum time was 48 h

in-vitro,

GBM,

U251

59.53 μM

n U251-MG cells, the optimum concentration of honokiol was 40 µM, and the optimum time was 48 h

AntiCan↑, In summary, studies have demonstrated that honokiol has multiple anticancer effects
TumCP↑, honokiol suppresses cell proliferation, and promotes autophagy and apoptosis
TumAuto↑,
Apoptosis↑,
*BioAv↑, honokiol could improve bioavailability in nerve tissue through passing the blood-brain barrie
*neuroP↑, honokiol has neuroprotective effects.
*NF-kB↑, honokiol could reduce cytokine production and stimulate glial nuclear factor kappa B (NFκB) to eliminate the inflammatory response during cerebral ischemia-reperfusion activity
MAPK↑, honokiol activated cells MAPK signaling pathway in human glioma cells
GPx4↑, The results showed that the ferroptosis-associated protein GPX4 was suppressed in honokiol-treated cells compared to control cells.
Tf↑, Ferroptosis-associated protein TF was upregulated in both honokiol-treated cell lines compared to the control
BAX↑, BAX was increased, and the expression of Bcl-2 was suppressed in both honokiol-treated cells, indicating that honokiol induced apoptosis in the human glioma cell lines U87-MG and U251-MG.
Bcl-2↓,
antiOx↑, Researchers have found that the antioxidant capacity of honokiol is 1000 times greater than that of vitamin E
Hif1a↓, reduce HIF-1α protein levels and suppress hypoxia-related signaling pathways
Ferroptosis↑, Honokiol activated ferroptosis in human glioma cells

4778-

Lyco,

Lycopene exerts cytotoxic effects by mitochondrial reactive oxygen species–induced apoptosis in glioblastoma multiforme

in-vitro,

GBM,

GBM8401

BBB↑, lycopene penetration across the blood-brain barrier and its induction of apoptosis, inhibiting proliferation in GBM8401 and T98G GBM cells
Apoptosis↑,
TumCP↑,
P53↑, lycopene promoted p53 upregulation and suppressed cyclins B and cyclin D, leading to cell cycle arrest through ROS-activated ERK pathways.
CycB/CCNB1↓,
cycD1/CCND1↓,
TumCCA↓,
mt-ROS↑, Lycopene induced Mito-ROS accumulation in GBM cells
TumCG↓, Lycopene inhibits the cell growth of GBM cells

5614-

NaHCO3,

Targeting the Acidic Tumor Microenvironment: Unexpected Pro-Neoplastic Effects of Oral NaHCO3 Therapy in Murine Breast Tissue

in-vivo,

BC,

NaHCO3-containing drinking water to female C57BL/6j mice. bc

e-pH↑, Oral NaHCO3 therapy increases breast tumor pH in vivo from 6.68 ± 0.04 to 7.04 ± 0.09 and intracellular pH in breast epithelial organoids by ~0.15.
TumCG↝, Breast tumors develop with median latency of 85.5 ± 8.2 days in NaHCO3-treated mice vs. 82 ± 7.5 days in control mice.
TumCP↑, accelerates proliferation without net effect on breast cancer development or tumor growth.

2078-

PB,

Butyrate-induced apoptosis in HCT116 colorectal cancer cells includes induction of a cell stress response

in-vitro,

CRC,

HCT116

0-20mM

p38↑, butyrate likely induces a cellular stress response in HCT116 cells characterized by p38 MAPK activation and an endoplasmic reticulum (ER) stress response, resulting in caspase 3/7 activation and cell death.
ER Stress↑,
Casp3↑,
Casp7↑,
TumCD↑,
Apoptosis↑, butyrate induces apoptosis and inhibits the proliferation of both HCT116 and HCT116-BR cells at concentrations of 2.5 mM and higher
TumCP↑,
HSP27↓, HSP27 is down-regulated in HCT116 cells following 48 h exposure to butyrate whereas in HCT116-BR cells, its expression remains relatively stable.

1132-

RT,

Rutin Promotes Proliferation and Orchestrates Epithelial–Mesenchymal Transition and Angiogenesis in MCF-7 and MDA-MB-231 Breast Cancer Cells

in-vitro,

BC,

MDA-MB-231

>100uM

rutin may act as a breast-cancer-promoting phytoestrogen.

in-vitro,

BC,

MCF7

Vim↑,
N-cadherin↑, CDH2
E-cadherin↓,
TumCP↑,
TumCMig↑,
tumCV↑, increased the number of viable cells at concentrations more than 200 µM.
MKI67↑, rutin (200 μM)

4718-

SSE,

High-Dose Selenium Induces Ferroptotic Cell Death in Ovarian Cancer

in-vitro,

Ovarian,

 SKOV3-bearing mice

TumCP↑, Here, we observed that high-dose sodium selenite (SS) significantly decreased the proliferation and increased the death of ovarian cancer cells, mediated by an increased generation of reactive oxygen species.
ROS↑,
GPx↓, high-dose SS decreased the levels of glutathione peroxidase (GPx), a selenoprotein with antioxidant properties, without altering other selenoproteins.
lipid-P↑, Furthermore, high-dose SS triggered lipid peroxidation and ferroptosis, a type of iron-dependent cell death, due to dysregulated GPx4 pathways.
Ferroptosis↑,
Dose↑, effective dose (1000–2000 μg/kg) of SS for anticancer effects in an ovarian cancer mouse model through tail injection three times per week for 2 weeks

6438-

T4O,

Terpinen-4-ol inhibits colorectal cancer growth via reactive oxygen species

in-vitro,

CRC,

HCT116

mt-ROS↑, TP4O induces apoptosis in CRC cells through ROS generation. TP4O were generated by mitochondria
TumCP↑, TP4O inhibited the proliferation of HCT116 xenografts compared with that of the control group
tumCV↑, TP4O inhibits CRC cell viability and proliferation
eff↓, CRC cells were exposed to specific antioxidants (NAC, EB and MnTBAP), which prevented significant TP4O-derived cell death (Fig. 5C), demonstrating that ROS accumulation was the cause for cell death.
TumVol↓, Mice treated with TP4O developed significantly smaller tumors
selectivity↑, results from the present study suggest that TP4O induces apoptosis in CRC cells through the generation of ROS in vitro and in vivo without damaging normal cells.

3747-

TTT,

Tumor treating induced fields: a new treatment option for patients with glioblastoma

in-vitro,

GBM,

U87MG

*TumCP↑, TTIF significantly inhibited the proliferation of U87 cells both in vitro and in vivo.

Showing Research Papers: 1 to 22 of 22

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 22

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome(tgid=24) ⓘ

CD8+↑, 1,
Total Targets: 148

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 3, NRF2↑, 1, ROS↓, 1,

Mitochondria & Bioenergetics(tgid=3) ⓘ

Insulin↑, 1,

Core Metabolism/Glycolysis(tgid=4) ⓘ

glucose↓, 1,

Cell Death(tgid=5) ⓘ

TRPV1↑, 1,

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

EMT↑, 1,

Migration(tgid=13) ⓘ

AntiAg↑, 1, TumCP↑, 1,

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 2, NF-kB↑, 1,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1, BioAv↑, 2, BioEnh↑, 1,

Clinical Biomarkers(tgid=22) ⓘ

BP↓, 1,

Functional Outcomes(tgid=23) ⓘ

chemoP↑, 1, neuroP↑, 2, Pain↓, 1,
Total Targets: 19

Scientific Paper Hit Count for: TumCP, Tumor Cell proliferation

2 Berberine
2 Capsaicin
2 Copper and Cu NanoParticles
1 alpha Linolenic acid
1 Artemisinin
1 Astaxanthin
1 5-fluorouracil
1 Beta-Caryophyllene
1 diet FMD Fasting Mimicking Diet
1 Disulfiram
1 Echinacea
1 EGCG (Epigallocatechin Gallate)
1 Quercetin
1 Emodin
1 Honokiol
1 Lycopene
1 Bicarbonate(Sodium)
1 Phenylbutyrate
1 Rutin
1 Selenite (Sodium)
1 Terpinen-4-ol / Tea Tree Oil
1 Tumor Treating Fields

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#:327  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

TumCP 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) ⓘ

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) ⓘ

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:

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

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

Migration(tgid=13) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

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