Database Query Results : Curcumin, , TumCG

CUR, Curcumin: Click to Expand ⟱

Features:

Curcumin is the main active ingredient in Tumeric. Member of the ginger family.Curcumin is a polyphenol extracted from turmeric with anti-inflammatory and antioxidant properties.
- Has iron-chelating, iron-chelating properties. Ferritin. But still known to increase Iron in Cancer cells.
- GSH depletion in cancer cells, exhaustion of the antioxidant defense system. But still raises GSH↑ in normal cells.
- Higher concentrations (5-10 μM) of curcumin induce autophagy and ROS production
- Inhibition of TrxR, shifting the enzyme from an antioxidant to a prooxidant
- Strong inhibitor of Glo-I, , causes depletion of cellular ATP and GSH
- Curcumin has been found to act as an activator of Nrf2, (maybe bad in cancer cells?), hence could be combined with Nrf2 knockdown
-may suppress CSC: suppresses self-renewal and pathways (Wnt/Notch/Hedgehog).
Clinical studies testing curcumin in cancer patients have used a range of dosages, often between 500 mg and 8 g per day; however, many studies note that doses on the lower end may not achieve sufficient plasma concentrations for a therapeutic anticancer effect in humans.
• Formulations designed to improve curcumin absorption (like curcumin combined with piperine, nanoparticle formulations, or liposomal curcumin) are often employed in clinical trials to enhance its bioavailability.

-Note half-life 6 hrs.
BioAv is poor, use piperine or other enhancers
Pathways:
- induce ROS production at high concentration. Lowers ROS at lower concentrations
curcumin can act as a pro-oxidant when blue light is applied
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: GSH↓ Catalase↓ HO1↓ GPx↓
but conversely is known as a NRF2↑ activator in cancer
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, uPA↓, VEGF↓, NF-κB↓, CXCR4↓, SDF1↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, HSP↓, Sp proteins↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, ERK↓, EMT↓, TOP1↓, TET1↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, HK2↓, ECAR↓, OXPHOS↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, CK2↓, Hh↓, GLi1↓, CD133↓, CD24↓, β-catenin↓, n-myc↓, sox2↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK↓, ERK↓, JNK, TrxR**,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Rank	Pathway / Axis	Cancer Cells	Normal Cells	Label	Primary Interpretation	Notes
1	NF-κB signaling	↓ NF-κB activation	↓ inflammatory NF-κB tone	Driver	Suppression of survival and inflammatory transcription	NF-κB is a primary, repeatedly validated curcumin target explaining pleiotropic downstream effects
2	STAT3 signaling	↓ STAT3 phosphorylation / activity	↔ or mild suppression	Driver	Loss of pro-survival and proliferative signaling	STAT3 inhibition contributes to growth arrest, apoptosis sensitization, and reduced cytokine signaling in tumors
3	Reactive oxygen species (ROS)	↑ ROS (dose- & context-dependent)	↓ ROS / buffered	Conditional Driver	Biphasic redox modulation	Curcumin can act as a pro-oxidant in cancer cells with high basal stress while acting antioxidant in normal cells
4	Mitochondrial integrity / intrinsic apoptosis	↓ ΔΨm; ↑ caspase activation	↔ preserved	Driver	Execution of intrinsic apoptosis	Mitochondrial dysfunction and caspase activation occur downstream of NF-κB/STAT3 and ROS effects
5	PI3K → AKT → mTOR axis	↓ AKT / ↓ mTOR	↔ or adaptive suppression	Secondary	Reduced growth and anabolic signaling	AKT/mTOR inhibition contributes to growth suppression and autophagy induction in cancer cells
6	Autophagy	↑ autophagy (protective or pro-death)	↑ adaptive autophagy	Secondary	Stress adaptation vs cell death	Autophagy may be cytoprotective or cooperate with apoptosis depending on context and dose
7	HIF-1α / VEGF hypoxia–angiogenesis axis	↓ HIF-1α; ↓ VEGF	↔ minimal effect	Secondary	Anti-angiogenic pressure	Suppression of hypoxia-driven transcription limits angiogenesis and tumor adaptation
8	Cell cycle regulation	↑ G2/M or G1 arrest	↔ largely spared	Phenotypic	Cytostatic growth control	Cell-cycle arrest reflects upstream signaling and epigenetic effects rather than direct CDK inhibition
9	Migration / invasion (EMT, MMP axis)	↓ migration & invasion	↔	Phenotypic	Anti-metastatic phenotype	Reduced EMT markers and protease activity limit invasive behavior
10	Epigenetic regulation (p300/CBP HAT activity)	↓ histone acetylation	↔ modest	Secondary	Transcriptional reprogramming	Curcumin modulates chromatin via HAT inhibition rather than classic HDAC inhibition

TumCG, Tumor cell growth: Click to Expand ⟱

Source:

Type:

Normal cells grow and divide in a regulated manner through the cell cycle, which consists of phases (G1, S, G2, and M).
Cancer cells often bypass these regulatory mechanisms, leading to uncontrolled proliferation. This can result from mutations in genes that control the cell cycle, such as oncogenes (which promote cell division) and tumor suppressor genes (which inhibit cell division).

Scientific Papers found: Click to Expand⟱

1024-

Api,

CUR,

Apigenin suppresses PD-L1 expression in melanoma and host dendritic cells to elicit synergistic therapeutic effects

vitro+vivo,

Melanoma,

A375

 (30 μM) for 24 h

in-vitro,

Melanoma,

A2058

in-vitro,

Melanoma,

RPMI-7951

TumCG↓,
Apoptosis↑,
PD-L1↓, IFN-γ-induced PD-L1 upregulation was significantly inhibited by flavonoids, especially apigenin
STAT1↓,
tumCV↓,
T-Cell↑, Curcumin and apigenin enhance T cell-mediated melanoma cell killing

1426-

Bos,

CUR,

Chemo,

Novel evidence for curcumin and boswellic acid induced chemoprevention through regulation of miR-34a and miR-27a in colorectal cancer

in-vivo,

CRC,

10um(cur), 30uM(AKBA)

mouse

in-vitro,

CRC,

HCT116

in-vitro,

CRC,

RKO

in-vitro,

CRC,

SW480

in-vitro,

RCC,

SW-620

in-vitro,

RCC,

HT-29

in-vitro,

CRC,

Caco-2

miR-34a↑, curcumin and AKBA induced upregulation of tumor-suppressive miR-34a and downregulation of miR-27a in CRC cells
miR-27a-3p↓,
TumCG↓,
BAX↑,
Bcl-2↓,
PARP1↓,
TumCCA↑,
Apoptosis↑,
cMyc↓,
CDK4↓,
CDK6↓,
cycD1/CCND1↓,
ChemoSen↑, combined treatment further increased the inhibitory effects
miR-34a↑, miR-34a expression was upregulated by curcumin and further elevated by concurrent treatment with curcumin and AKBA in HCT116 cell
miR-27a-3p↓,

2015-

CAP,

CUR,

urea,

Anti-cancer Activity of Sustained Release Capsaicin Formulations

Review,

Var,

AntiCan↑, Several convergent studies show that capsaicin displays robust cancer activity, suppressing the growth, angiogenesis and metastasis of several human cancers.
TumCG↓,
angioG↓,
TumMeta↓,
BioAv↓, clinical applications of capsaicin as a viable anti-cancer drug have remained problematic due to its poor bioavailability and aqueous solubility properties
BioAv↓, capsaicin is associated with adverse side effects like gastrointestinal cramps, stomach pain, nausea and diarrhea and vomiting
BioAv↑, All these hurdles may be circumvented by encapsulation of capsaicin in sustained release drug delivery systems.
selectivity↑, Most importantly, these long-acting capsaicin formulations selectively kill cancer cells and have minimal growth-suppressive activity on normal cells.
EPR↑, The EPR effect is a mechanism by which high–molecular drug delivery systems (typically prodrugs, liposomes, nanoparticles, and macromolecular drugs) tend to accumulate in tumor tissue much more than they do in normal tissues
eff↓, The efficiency of such extravasation is maximum when the size of the liposomes less than 200 nm The CAP-CUR-GLY-GAL-LIPO were spherical in shape with a narrow range of size distribution ranging from 135–155nm
ChemoSen↑, The chemosensitization and anti-tumor activity of capsaicin involves multiple molecular pathways
Dose∅, oral, Intravenous (IV), and Intraperitoneal (IP) options
Half-Life∅, oral metabolized in 105mins, T1/2in blood=25mins.
eff↑, presence of urea (as a carrier) increased the aqueous solubility of capsaicin by 3.6-fold compared to pure capsaicin

4676-

CUR,

Curcumin suppresses stem-like traits of lung cancer cells via inhibiting the JAK2/STAT3 signaling pathway

vitro+vivo,

Lung,

H460

CSCs↓, In the present study, we tested the effects of curcumin on lung cancer stem-like cells and report that in addition to inhibition on the proliferation and colony formation of lung cancer cells, curcumin reduces tumor spheres of H460 cells
JAK2↓, via inhibiting the JAK2/STAT3 signaling pathway
STAT3↓,
TumCP↓, Curcumin inhibits proliferation and colony formation of NCI-H460 lung cancer cells.
TumCG↓, Curcumin inhibits tumor spheres growth of NCI-H460 lung cancer cells in vivo.

4830-

CUR,

Curcumin and Its Derivatives Induce Apoptosis in Human Cancer Cells by Mobilizing and Redox Cycling Genomic Copper Ions

in-vitro,

Var,

eff↑, intracellular copper reacts with curcuminoids in cancer cells to cause DNA damage via ROS generation.
ROS↑, Apoptosis of Cancer Cells Induced by Curcumin Is Mediated by ROS
DNAdam↑,
TumCG↓, Curcumin Inhibits Growth and Induces Apoptosis in Different Types of Cancer Cells
Apoptosis↑,
eff↓, Curcumin-Induced Antiproliferation and Apoptosis in Cancer Cells Are Inhibited by a Cuprous Chelator but Not by Iron and Zinc Chelators
Fenton↑, Generation of superoxide anions may spontaneously result in the synthesis of H2O2, which in turn results in the formation of hydroxyl radicals via oxidation of reduced copper (Fenton reaction)
eff↑, Copper Supplementation Increases the Sensitivity of Normal Breast Epithelial Cells to the Antiproliferative Effects of Curcumin

4671-

CUR,

Targeting colorectal cancer stem cells using curcumin and curcumin analogues: insights into the mechanism of the therapeutic efficacy

in-vitro,

CRC,

CSCs↓, Intriguingly, curcumin and its analogues have also recently been shown to be effective in lowering tumour recurrence by targeting the CSC population, hence inhibiting tumour growth.
TumCG↓,
ChemoSen↑, curcumin could play a role as chemosensitiser whereby the colorectal CSCs are now sensitised towards the anti-cancer therapy,
Wnt↓, Three major signaling pathways in which curcumin plays a pivotal role in CSC self-renewal behavior are the Wnt/β-catenin, Sonic Hedgehog (SHH), and Notch pathways
β-catenin/ZEB1↓,
Shh↓,
NOTCH↓,
DNMT1↓, Figure 1
STAT3↓,
NF-kB↓,
EGFR↓,
IGFR↓,
TumCCA↓,
cl‑PARP↑,
BAX↑,
ECM/TCF↓,

2974-

CUR,

Curcumin Suppresses Metastasis via Sp-1, FAK Inhibition, and E-Cadherin Upregulation in Colorectal Cancer

in-vitro,

CRC,

HCT116

0, 5, 10, and 20 μM

in-vitro,

CRC,

HT29

in-vitro,

CRC,

HCT15

in-vitro,

CRC,

COLO205

in-vitro,

CRC,

SW-620

in-vivo,

NA,

1 g/kg once daily for 30 days

mice

TumCMig↓, Curcumin significantly inhibits cell migration, invasion, and colony formation in vitro and reduces tumor growth and liver metastasis in vivo.
TumCI↓,
TumCG↓,
TumMeta↓,
Sp1/3/4↓, curcumin suppresses Sp-1 transcriptional activity and Sp-1 regulated genes including ADEM10, calmodulin, EPHB2, HDAC4, and SEPP1 in CRC cells.
HDAC4↓,
FAK↓, Curcumin inhibits focal adhesion kinase (FAK) phosphorylation
CD24↓, Curcumin reduces CD24 expression in a dose-dependent manner in CRC cells
E-cadherin↑, E-cadherin expression is upregulated by curcumin and serves as an inhibitor of EMT.
EMT↓,
TumCP↓,
NF-kB↓, CUR prevents cancer cells migration, invasion, and metastasis through inhibition of PKC, FAK, NF-κB, p65, RhoA, MMP-2, and MMP-7 gene expressions
AP-1↝,
STAT3↓, downregulation of CD24 reduces STAT and FAK activity, decreases cell proliferation, metastasis in human tumor
P53?,
β-catenin/ZEB1↓, CUR could activate protein kinase D1 (PKD1) suggesting that suppressing of β-catenin transcriptional activity prevents growth of prostate cancer
NOTCH1↝,
Hif1a↝,
PPARα↝,
Rho↓, CUR prevents cancer cells migration, invasion, and metastasis through inhibition of PKC, FAK, NF-κB, p65, RhoA, MMP-2, and MMP-7 gene expressions
MMP2↓,
MMP9↓,

3578-

CUR,

SIL,

Curcumin, but not its degradation products, in combination with silibinin is primarily responsible for the inhibition of colon cancer cell proliferation

in-vitro,

CRC,

DLD1

eff↑, combination of curcumin and silymarin exhibited synergistic anticancer activity.
BioAv↓, Despite the low bioavailability of curcumin and the relatively low daily dietary intake (Shen et al. 2016, Teiten et al. 2010, Tsuda 2018), the beneficial effect of curcumin observed could be due to other phytochemicals present in the diet and act sy
TumCG↓, curcumin and silibinin in combination inhibit cell growth significantly

2980-

CUR,

Inhibition of NF B and Pancreatic Cancer Cell and Tumor Growth by Curcumin Is Dependent on Specificity Protein Down-regulation

in-vivo,

PC,

mice

TumCG↓, curcumin inhibits Panc28 and L3.6pL pancreatic cancer cell and tumor growth in nude mice bearing L3.6pL cells as xenografts
p50↓, curcumin decreased expression of p50 and p65 proteins and NFkappaB-dependent transactivation and also decreased Sp1, Sp3, and Sp4 transcription factor
p65↓,
NF-kB↓,
Sp1/3/4↓,
MMP↓, Curcumin also decreased mitochondrial membrane potential and induced reactive oxygen species in pancreatic cancer cell
ROS↑,

465-

CUR,

Curcumin inhibits the growth of liver cancer by impairing myeloid-derived suppressor cells in murine tumor tissues

vitro+vivo,

Liver,

HepG2

1.2, 2.4, 4.8 and 9.6 µg/mL, 24 and 48 h; 120 and 240 mg/kg/day, 15 days

vitro+vivo,

Liver,

HUH7

vitro+vivo,

Liver,

MHCC-97H

TumCG↓,
MDSCs↓,
TLR4↓,
NF-kB↓,
IL6↓,
IL1↓, IL-1β
PGE2↓,
COX2↓,
GM-CSF↓,
angioG↓,
VEGF↓,
CD31↓,
GM-CSF↓,
α-SMA↓,
p‑IKKα↓, p-IKKα, p-IKKβ
MyD88↓,

451-

CUR,

The effect of Curcumin on multi-level immune checkpoint blockade and T cell dysfunction in head and neck cancer

vitro+vivo,

HNSCC,

SCC15

1, 2, 5, 10, 20, 40 and 80 µM, 1, 3, 6, 12 and 24 h; 50 mg/kg, 6 weeks

vitro+vivo,

HNSCC,

SNU1076

vitro+vivo,

HNSCC,

SNU1041

TumCMig↓,
TumCG↓,
PD-L1↓,
PD-L2↓,
Galectin-9↓,
EMT↓,
T-Cell↑,
TILs↑,
PD-1↓,
TIM-3↓,
CD4+↓,
CD25+↓,
FoxP3+↓,
E-cadherin↑,
CD8+↑,
IFN-γ↑,

1409-

CUR,

Curcumin analog WZ26 induces ROS and cell death via inhibition of STAT3 in cholangiocarcinoma

in-vivo,

CCA,

Walker256

mouse

TumCG↓,
ROS↑,
MMP↓,
STAT3↓,
TumCCA↑, G2/M cell cycle
eff↓, Pretreatment of N-acetyl cysteine (NAC), an antioxidant agent, could fully reverse the WZ26-induced ROS-mediated changes in CCA cells

1410-

CUR,

Curcumin induces ferroptosis and apoptosis in osteosarcoma cells by regulating Nrf2/GPX4 signaling pathway

vitro+vivo,

OS,

MG63

tumCV↓,
Apoptosis↑,
TumCG↓,
NRF2↓, after treatment with curcumin, Nrf2 and GPX4 levels were significantly decreased
GPx4↓,
HO-1↓,
xCT↓, SLC7A11
ROS↑, our results revealed that after treatment with curcumin, ROS and MDA levels were significantly increased while GSH levels were decreased
MDA↑,
GSH↓,

482-

CUR,

PDT,

The Antitumor Effect of Curcumin in Urothelial Cancer Cells Is Enhanced by Light Exposure In Vitro

in-vitro,

Bladder,

RT112

0.1 to 0.4 μg/ml

in-vitro,

Bladder,

UMUC3

Apoptosis↑, cur + light only
TumCG↓,
TumCP↓,

131-

CUR,

Modulation of AKR1C2 by curcumin decreases testosterone production in prostate cancer

vitro+vivo,

Pca,

LNCaP

 5, 25 and 50 μM, 24, 48 and 72 h; 200 mg/kg/day, 30days

 mice

vitro+vivo,

Pca,

22Rv1

AKR1C2↓, Curcumin upregulated AKR1C2 expression in LNCaP. by approximately 170‐fold at 50 μmol/L
CYP11A1↓, CYP11A1 and HSD3B2 were significantly decreased.
HSD3B↓,
DHT↓,
testos↓,
StAR↓,
SRD5A1↑,
AR↓, suggest that curcumin's natural bioactive compounds could have potent anticancer properties due to suppression of androgen production,
tumCV↓, cell viability of LNCaP decreased by 50% when 5 μmol/L of curcumin was added to the culture medium.
TumCG↓, 50 μmol/L of curcumin completely inhibit the growth of 22Rv1 cells.
Apoptosis↑, Induction of apoptosis after curcumin treatment

134-

CUR,

RES,

MEL,

SIL,

Thioredoxin 1 modulates apoptosis induced by bioactive compounds in prostate cancer cells

in-vitro,

Pca,

LNCaP

in-vitro,

Pca,

PC3

Apoptosis↑,
ROS↑, curcumin and resveratrol promote ROS production and induce apoptosis in LNCaP and PC-3.
Trx1↓, Melatonin and silibinin did not change the basal redox state in LNCaP and these compounds even caused a further TRX1 reduction in PC-3 cells.
TumCG↓, Melatonin and silibinin inhibit cell growth while curcumin and resveratrol induce apoptosis in prostate cancer cell
eff↓, NAC prevents curcumin-induced apoptosis
TXNIP↑, Resveratrol decreases TRX1 by increasing TXNIP mRNA levels in PC-3 cells.

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↑,

144-

CUR,

Bical,

Combination of curcumin and bicalutamide enhanced the growth inhibition of androgen-independent prostate cancer cells through SAPK/JNK and MEK/ERK1/2-mediated targeting NF-κB/p65 and MUC1-C

in-vitro,

Pca,

PC3

 androgen-independent prostate cancer cells

in-vitro,

PC,

DU145

in-vitro,

PC,

LNCaP

p‑ERK↑, ERK1/2
p‑JNK↓, phosphorylation
MUC1↓, MUC1-C protein expression
p65↓,
AR↓, bicalutamide, an androgen receptor antagonist, inhibited cell growth in dose- and time-dependent fashion in PC3 and LNCaP cells.
TumCG↓,
MEK↑, curcumin inhibits the growth of androgen-independent prostate cancer cells through MEK/ERK1/2 and SAPK/JNK-mediated inhibition of p65, followed by reducing expression of MUC1-C protein.
SAPK↑, through activation of MEK/ERK/12 and SAPK/JNK

152-

CUR,

Anti-cancer activity of curcumin loaded nanoparticles in prostate cancer

in-vivo,

Pca,

 PLGA-CUR NPs

 mice

β-catenin/ZEB1↓,
AR↓, Treatment with PLGA-CUR NPs drastically decreases the AR expression level (Figure 5C) compared to free curcumin.
STAT3↓, PLGA-CUR treatment inhibited the expression of STAT3 and phosphorylation of AKT at even the lowest concentration
p‑Akt↓,
Mcl-1↓,
Bcl-xL↓,
cl‑PARP↑, Prostate cancer cells treated with CUR or PLGA-CUR NPs exhibited PARP cleavage and inhibited the expression of anti-apoptotic proteins, Bcl-XL and Mcl-1
miR-21↓, 9-fold reduction in expression of the oncomir, miR-21, in prostate cancer cells (C4-2 and DU-145) t
miR-205↑,
TumCG↓, PLGA-CUR NPs were capable of reducing both in vitro and in vivo prostate cancer cell growth,
TumCP↓, data suggest that curcumin can effectively suppress prostate cancer cell proliferation, invasion, angiogenesis, and metastasis
TumCI↓,
angioG↓,
TumMeta↓,

154-

CUR,

Curcumin inhibits expression of inhibitor of DNA binding 1 in PC3 cells and xenografts

vitro+vivo,

Pca,

PC3

Id1↓, significant decrease in the mRNA and protein expression of Id1
TumCG↓, Tumor growth in mice was obviously suppressed by curcumin during the period of 24 to 30 days.

126-

CUR,

Modulation of miR-34a in curcumin-induced antiproliferation of prostate cancer cells

in-vitro,

Pca,

22Rv1

 1, 5, 10 and 20 μM, 4 days

in-vitro,

Pca,

PC3

in-vitro,

Pca,

DU145

miR-34a↑, curcumin significantly upregulated the expression of miR‐34a, along with the downregulated expression of β‐catenin and c‐myc in three prostate cancer cell lines.
β-catenin/ZEB1↓, curcumin‐induced miR‐34a suppressed the activation of β‐catenin/c‐myc axis and inhibited cell proliferation of prostate cancer cells.
cMyc↓,
P21↑,
cycD1/CCND1↓,
PCNA↓,
TumCG↓, Curcumin inhibited cell growth of prostate cancer cells

129-

CUR,

Curcumin suppressed the prostate cancer by inhibiting JNK pathways via epigenetic regulation

vitro+vivo,

Pca,

LNCaP

JNK↓, curcumin inhibits JNK pathway and plays a role in epigenetic regulation of prostate cancer cells by repressing H3K4me3.
H3K4↓,
TumCG↓, Curcumin inhibits growth of prostate cancer in vivo
Apoptosis↑, Curcumin promoted apoptosis of LNCaP cells in vitro
eff↑, Combination of curcumin and JQ-1 inhibited the prostate cancer efficiently

404-

CUR,

Curcumin induces ferroptosis in non-small-cell lung cancer via activating autophagy

vitro+vivo,

Lung,

A549

mice

vitro+vivo,

Lung,

H1299

TumAuto↑,
TumCG↓,
TumCP↓,
Iron↑, iron overload
GSH↓, GSH depletion
lipid-P↑, accumulation of intracellular iron and lipid‐reactive oxygen species (ROS), lipid peroxidation
GPx↓, GPX4
mtDam↑, mitochondrial membrane rupture
autolysosome↑,
Beclin-1↑,
LC3s↑,
p62↓,
Ferroptosis↑, via activating autophagy

164-

CUR,

Anti-tumor activity of curcumin against androgen-independent prostate cancer cells via inhibition of NF-κB and AP-1 pathway in vitro

in-vitro,

Pca,

PC3

NF-kB↓, via Inhibition of NF-κB and AP-1 Pathway in vitro
AP-1↓,
TumCG↓, Curcumin could effectively suppress the in vitro growth of PC-3 cells.
TumCCA↑, Curcumin treatment significantly arrested PC-3 cells in the G 2/M phase

156-

Ralox,

Tam,

GEN,

CUR,

Modulators of estrogen receptor inhibit proliferation and migration of prostate cancer cells

in-vitro,

Pca,

DU145

in-vitro,

Pca,

PC3

ERβ/ESR2↑,
TumCG↓, Regulation of PC cell growth by raloxifen, tamoxifen, genistein and curcumin
TumCMig↓, genistein and curcumin reduced the migratory activity of DU145 cells by 43% and 25%, respectively; for PC3 cells the reduction was about 40%
FAK↓, genistein seemed to be an inhibition of the activation of Focal Adhesion Kinase (FAK) and mitogen-activated kinase (MAPK) p38-heat shock protein 27 that mediates detachment and cellular migration respectively
p38↓,

139-

Tomatine,

CUR,

Combination of α-Tomatine and Curcumin Inhibits Growth and Induces Apoptosis in Human Prostate Cancer Cells

in-vitro,

Pca,

PC3

NF-kB↓, synergistic inhibition of NF-κB activity and a potent decrease in the expression of its downstream gene Bcl-2 in the cells.
Bcl-2↓,
p‑Akt↓, strong decreases in the levels of phospho-Akt and phosphor-ERK1/2 were found in PC-3 cells treated with α-tomatine and curcumin in combination
p‑ERK↓, ERK1/2
TumCG↓, α-tomatine in combination with curcumin may be an effective strategy for inhibiting the growth of prostate cancer.
Apoptosis↑, α-Tomatine and curcumin induce apoptosis in PC-3 cells
PCNA↓, Combined treatment with α-tomatine and curcumin had a more potent effect on decreasing the number of PCNA positive cells than either agent used alone
BioAv↓, However, the bioavailability of curcumin is low

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 26

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

CD8+↑, 1,
Total Targets: 141

Pathway results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: TumCG, Tumor cell growth

26 Curcumin
2 Silymarin (Milk Thistle) silibinin
1 Apigenin (mainly Parsley)
1 Boswellia (frankincense)
1 Chemotherapy
1 Capsaicin
1 urea
1 Photodynamic Therapy
1 Resveratrol
1 Melatonin
1 Bicalutamide
1 raloxifen
1 tamoxifen
1 Genistein (soy isoflavone)
1 Tomatine

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#:65  Target#:323  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

Database Query Results : Curcumin, , TumCG

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned ⓘ

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Cellular Microenvironment ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

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