Curcumin / PARP Cancer Research Results

CUR, Curcumin: Click to Expand ⟱
Features:
Curcumin is the main active ingredient in Turmeric. 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).

Curcumin — Curcumin is a turmeric-derived polyphenolic curcuminoid and diarylheptanoid from Curcuma longa, functionally best classified as a natural-product small molecule / nutraceutical candidate with pleiotropic redox, inflammatory, transcriptional, metabolic, and chemosensitizing activity. The standard abbreviation is CUR. It is the principal active pigment of turmeric rhizome, usually studied as purified curcumin, curcuminoid mixtures, turmeric extract, phytosomal curcumin, liposomal curcumin, nanoparticle curcumin, or piperine-enhanced formulations. Its oncology relevance is mechanistically broad but clinically constrained by poor aqueous solubility, rapid metabolism, low free systemic exposure, formulation variability, and insufficient well-powered cancer outcome trials.

Primary mechanisms (ranked):

  1. Suppression of NF-κB / STAT3 inflammatory-survival signaling, reducing cytokine, COX-2, iNOS, anti-apoptotic, invasion, and treatment-resistance programs.
  2. Biphasic redox modulation: ROS buffering in normal/inflamed tissue but ROS↑, GSH depletion, thioredoxin reductase disruption, and oxidative stress amplification in susceptible cancer models at sufficient exposure.
  3. Mitochondrial injury and intrinsic apoptosis, including mitochondrial membrane potential loss, cytochrome-c release, caspase activation, PARP cleavage, and ER-stress/UPR involvement.
  4. PI3K/AKT/mTOR and MAPK pathway modulation, contributing to growth arrest, autophagy modulation, apoptosis sensitization, and reduced survival signaling.
  5. Wnt/β-catenin, Hedgehog/GLI, Notch, and cancer-stem-cell suppression, reducing stemness, EMT, invasion, and recurrence-associated phenotypes in models.
  6. Hypoxia / HIF-1α and glycolysis inhibition, including reduced GLUT1, HK2, LDHA, PKM2, lactate/ECAR, and Warburg-like metabolic support in selected models.
  7. Anti-angiogenic and anti-metastatic modulation, including VEGF, MMPs, uPA, CXCR4/SDF-1, TGF-β/α-SMA, FAK, and EMT-related axes.
  8. Epigenetic and transcriptional reprogramming, including reported HDAC, DNMT, EZH2, Sp-family, p53, and microRNA-related effects.
  9. NRF2 modulation: generally cytoprotective in normal cells but potentially protective for cancer cells when NRF2 is activated; NRF2 suppression/knockdown can increase curcumin-induced ROS stress in some tumor models.
  10. Chemosensitization and radiosensitization, with parallel normal-tissue protective signals reported in some mucositis, dermatitis, oxidative-stress, and radioprotection contexts.

Bioavailability / PK relevance: Conventional oral curcumin has poor systemic bioavailability because of low solubility, low absorption, rapid conjugation, and rapid elimination. Oral trials have used doses up to gram-level daily dosing, but circulating free curcumin is typically low; measured plasma exposure often reflects conjugated curcumin. Piperine, phospholipid/phytosome, micellar, liposomal, nanoparticle, and other enhanced formulations can raise exposure, but each formulation should be treated as a distinct translational entity. Delivery constraints are central for oncology interpretation.

In-vitro vs systemic exposure relevance: Common in-vitro anticancer concentrations, often in the low-to-mid micromolar range and sometimes higher, frequently exceed achievable free plasma exposure from standard oral curcumin. Therefore, direct systemic anticancer claims from cell culture should be weighted cautiously unless supported by tissue-local exposure, enhanced formulation data, local delivery, IV/liposomal delivery, or clinically measured pharmacodynamic biomarkers.

Clinical evidence status: Preclinical evidence is extensive; human oncology evidence is mainly small human, biomarker, pilot, chemoprevention, adjunctive, symptom-management, and formulation trials. Current authoritative oncology summaries judge evidence inadequate to recommend curcumin-containing products as cancer treatment or as routine adjunct anticancer therapy, although symptom-support areas such as oral mucositis, radiation dermatitis, oxidative-status measures, and quality of life have more suggestive but still confirmatory-level evidence.


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

Curcumin Cancer Mechanism Ranking

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 NF-κB / STAT3 inflammatory survival signaling NF-κB ↓; STAT3 ↓; IL-6/TNF-α/COX-2/iNOS ↓; Bcl-2/Bcl-xL/survivin programs ↓ Inflammatory tone ↓; tissue-protective anti-inflammatory effect likely context-dependent R/G Reduced survival, inflammation, invasion, and therapy-resistance signaling Most central and industry-relevant axis; explains many downstream effects but is not curcumin-specific.
2 Biphasic redox stress and antioxidant buffering ROS ↑ (dose-dependent); GSH ↓; antioxidant reserve ↓; oxidative apoptosis ↑ ROS ↓; NRF2/SOD/GSH/catalase/HO-1 often ↑ in stress models R/G Selective redox pressure in susceptible tumor cells with normal-cell protection in lower-stress settings Direction depends strongly on concentration, formulation, light exposure, basal redox state, and tumor antioxidant capacity.
3 Thioredoxin reductase and GSH linked redox systems TrxR inhibition or redox cycling ↑; GSH depletion ↑; oxidative stress ↑ Usually buffered or antioxidant response ↑ at non-toxic exposure R/G Collapse of tumor redox compensation Mechanistically important for ROS amplification and radiosensitization; achievable exposure remains a major constraint.
4 Mitochondrial depolarization and intrinsic apoptosis ΔΨm ↓; cytochrome-c ↑; caspase-3/9 ↑; PARP cleavage ↑; apoptosis ↑ Generally ↔ or protected under oxidative/inflammatory stress R/G Execution of apoptosis after upstream redox and survival-signal disruption Central cytotoxic endpoint in many cell models; often downstream of ROS, ER stress, AKT/mTOR suppression, or p53 modulation.
5 PI3K / AKT / mTOR and autophagy balance PI3K ↓; AKT ↓; mTOR ↓; survival signaling ↓; autophagy ↑ or mixed Stress-adaptive autophagy ↔ or ↑ (context-dependent) R/G Growth suppression and apoptosis sensitization Autophagy may be cytotoxic or protective depending on model and timing; combination logic may require autophagy-state interpretation.
6 Wnt / β-catenin / Hedgehog / Notch stemness signaling β-catenin ↓; GLI/Hedgehog ↓; Notch ↓; CD133/CD44/OCT4/SOX2-like stemness markers ↓ Generally ↔; possible normal stem-cell effects are tissue/context-dependent G Reduced cancer stemness, EMT, self-renewal, and recurrence-associated phenotypes Important for anti-metastatic and anti-CSC positioning; evidence is mainly preclinical.
7 HIF-1α / glycolysis / Warburg metabolism HIF-1α ↓; GLUT1 ↓; HK2 ↓; LDHA ↓; PKM2 ↓; lactate/ECAR ↓; ATP stress ↑ Metabolic effects ↔ or adaptive; normal-cell toxicity depends on exposure G Reduced hypoxic adaptation and glycolytic energy support Mechanistically relevant but formulation and tissue exposure are critical; hypoxic tumors may be more relevant than normoxic cell culture.
8 EMT / invasion / metastasis matrix axis EMT ↓; MMP2/MMP9 ↓; uPA ↓; FAK ↓; CXCR4/SDF-1 ↓; migration/invasion ↓ Inflammation-linked remodeling ↓; wound-healing effects context-dependent G Anti-invasive and anti-metastatic phenotype Strongly supported in models; clinical anti-metastatic efficacy is not established.
9 VEGF / angiogenesis / hypoxia interface VEGF ↓; HIF-1α ↓; angiogenic signaling ↓ Angiogenesis modulation ↔ or ↓ (context-dependent) G Reduced tumor vascular-support signaling Overlaps with NF-κB, HIF-1α, STAT3, and inflammatory cytokine suppression.
10 Epigenetic and transcriptional reprogramming HDAC ↓; DNMT1/3A ↓; EZH2 ↓; Sp proteins ↓; p53 ↑ or restored in selected models Broad transcriptional effects possible; selectivity uncertain G Reactivation of growth-control and differentiation-associated programs Biologically plausible but highly model-dependent; direct target specificity is lower than pathway-level interpretation.
11 Ferroptosis and iron redox stress Iron/redox stress ↑; lipid peroxidation ↑; GPX4/GSH axis may ↓ (model-dependent) Iron-chelation and antioxidant protection may occur (context-dependent) R/G Potential ferroptosis contribution in susceptible tumor models Curcumin can behave as an iron chelator, antioxidant, or pro-oxidant depending on exposure, formulation, and cancer redox context.
12 NRF2 cytoprotection risk NRF2 ↑ may protect tumor cells; NRF2 depletion can enhance curcumin-induced ROS stress in some models NRF2 ↑ supports antioxidant and anti-inflammatory tissue protection G Dual-edged stress-response modulation Important caution for antioxidant matrix use: NRF2 activation is favorable in normal-cell protection but may be undesirable in NRF2-addicted tumors.
13 Chemosensitization and radiosensitization Chemo response ↑; radiation response ↑; apoptosis ↑; resistance pathways ↓ Chemo/radiation injury may ↓ in mucositis, dermatitis, and oxidative-stress contexts R/G Adjunct sensitization with possible normal-tissue protection Attractive translational axis, but clinical evidence remains mainly pilot/small-study; interaction risk should be checked per regimen.
14 Clinical Translation Constraint Free systemic exposure often insufficient for direct cytotoxic extrapolation from in-vitro micromolar data Enhanced formulations may improve exposure but may also alter safety, liver-risk profile, and interaction potential G Bioavailability and formulation dominate translational interpretation Separate ordinary curcumin, turmeric extract, piperine-enhanced, phytosomal, micellar, liposomal, nanoparticle, and IV/liposomal products where possible.

TSF legend:

P: 0–30 min

R: 30 min–3 hr

G: >3 hr
PARP, poly ADP-ribose polymerase (PARP) cleavage: Click to Expand ⟱
Source:
Type:
Poly (ADP-ribose) polymerase (PARP) cleavage is a hallmark of caspase activation. PARP (Poly (ADP-ribose) polymerase) is a family of proteins involved in a variety of cellular processes, including DNA repair, genomic stability, and programmed cell death. PARP enzymes play a crucial role in repairing single-strand breaks in DNA.
PARP has gained significant attention, particularly in the treatment of certain types of tumors, such as those with BRCA1 or BRCA2 mutations. These mutations impair the cell's ability to repair double-strand breaks in DNA through homologous recombination. Cancer cells with these mutations can become reliant on PARP for survival, making them particularly sensitive to PARP inhibitors.
PARP inhibitors, such as olaparib, rucaparib, and niraparib, have been developed as targeted therapies for cancers associated with BRCA mutations.

PARP Family:
The poly (ADP-ribose) polymerases (PARPs) are a family of enzymes involved in a number of cellular processes, including DNA repair, genomic stability, and programmed cell death.
PARP1 is the predominant family member responsible for detecting DNA strand breaks and initiating repair processes, especially through base excision repair (BER).

PARP1 Overexpression:
In several cancer types—including breast, ovarian, prostate, and lung cancers—elevated PARP1 expression and/or activity has been reported.
High PARP1 expression in certain cancers has been associated with aggressive tumor behavior and resistance to therapies (especially those that induce DNA damage).
Increased PARP1 activity may correlate with poorer overall survival in tumors that rely on DNA repair for survival.
Scientific Papers found: Click to Expand⟱
4671- CUR,    Targeting colorectal cancer stem cells using curcumin and curcumin analogues: insights into the mechanism of the therapeutic efficacy
- in-vitro, CRC, NA
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↓,

6227- CUR,    Revisiting Curcumin in Cancer Therapy: Recent Insights into Molecular Mechanisms, Nanoformulations, and Synergistic Combinations
- Review, Var, NA
Wnt↓, By targeting multiple molecular pathways, including Wnt/β-catenin, PI3K/Akt/mTOR, JAK/STAT3, MAPK, NF-κB, and Notch, curcumin suppresses cancer growth and induces apoptosis.
β-catenin/ZEB1↓,
PI3K↓,
Akt↓,
mTOR↓,
JAK↓,
STAT3↓,
MAPK↓,
NF-kB↓,
NOTCH↓,
TumCG↓,
Apoptosis↑,
GSK‐3β↓, curcumin directly targets β-catenin and key Wnt/β-catenin regulators, including Dvl-2, Dvl-3, and GSK-3β.
cMyc↓, curcumin downregulates downstream oncogenic effectors such as c-Myc and Survivin while upregulating Axin-2, thereby inducing G2/M cell cycle arrest and apoptosis.
survivin↓,
Axin2↑,
TumCCA↑,
PTEN↑, curcumin upregulates PTEN expression, restoring its negative regulatory effect on the PI3K/Akt pathway.
P53↑, Curcumin’s activation and stabilization of p53 have been demonstrated in multiple cancer cell lines
ROS↑, In cervical cancer cells, curcumin induced apoptosis and ROS accumulation. Curcumin treatment elevated cleaved caspase-3 and PARP levels, markers of apoptosis.
Casp3↑,
PARP↑,
Ferroptosis↑, Ferroptosis Induction by Curcumin
angioG↓, Curcumin Inhibits Angiogenesis, Invasion, and Metastasis in Cancer Cells
TumCI↓,
TumMeta↓,
BioAv↓, curcumin’s clinical translation is limited by its poor bioavailability, rapid metabolism, and low systemic stability.
Half-Life↓,
ChemoSen↑, Synergistic Effects of Curcumin with Chemotherapy and Nanoparticle-Based Drug Delivery Systems

457- CUR,    Curcumin regulates proliferation, autophagy, and apoptosis in gastric cancer cells by affecting PI3K and P53 signaling
- in-vitro, GC, SGC-7901 - in-vitro, GC, BGC-823
TumCP↓,
Apoptosis↑,
TumAuto↑,
P53↑,
PI3K↓,
P21↑,
p‑Akt↓,
p‑mTOR↓,
Bcl-2↓,
Bcl-xL↓,
LC3I↓, LC3I
BAX↑,
Beclin-1↑,
cl‑Casp3↑,
cl‑PARP↑,
LC3II↑,
ATG3↑,
ATG5↑,

462- CUR,    Curcumin promotes cancer-associated fibroblasts apoptosis via ROS-mediated endoplasmic reticulum stress
- in-vitro, Pca, PC3
Bcl-2↓,
MMP↓,
cl‑Casp3↑,
BAX↑,
BIM↑,
p‑PARP↑,
PUMA↑,
p‑P53↑,
ROS↑,
p‑ERK↑,
p‑eIF2α↑,
CHOP↑,
ATF4↑,

471- CUR,    Curcumin induces apoptotic cell death and protective autophagy by inhibiting AKT/mTOR/p70S6K pathway in human ovarian cancer cells
- in-vitro, Ovarian, SKOV3 - in-vitro, Ovarian, A2780S
Apoptosis↑,
TumAuto↑,
p62↓,
p‑Akt↓,
p‑mTOR↓,
p‑P70S6K↓,
Casp9↑,
PARP↑,
ATG3↑,
Beclin-1↑,
LC3‑Ⅱ/LC3‑Ⅰ↑,

434- CUR,    Curcumin induces apoptosis in lung cancer cells by 14-3-3 protein-mediated activation of Bad
- in-vitro, Lung, A549
14-3-3 proteins↓,
p‑BAD↓, p-Bad
p‑Akt↓,
Akt↓,
cl‑Casp9↑, cleaved
cl‑PARP↑, cleaved

448- CUR,    Heat shock protein 27 influences the anti-cancer effect of curcumin in colon cancer cells through ROS production and autophagy activation
- in-vitro, CRC, HT-29
Apoptosis↑,
TumCCA↑, G2/M cell cycle arrest
p‑Akt↓,
Akt↓,
Bcl-2↓,
p‑BAD↓,
BAD↑,
cl‑PARP↑,
ROS↑,
HSP27↑,
Beclin-1↑,
p62↑,
GPx1↓,
GPx4↓,

1980- CUR,  Rad,    Thioredoxin reductase-1 (TxnRd1) mediates curcumin-induced radiosensitization of squamous carcinoma cells
- in-vitro, Cerv, HeLa - in-vitro, Laryn, FaDu
selectivity↑, previously demonstrated that curcumin radiosensitizes cervical tumor cells without increasing the cytotoxic effects of radiation on normal human fibroblasts
RadioS↑,
TrxR↓, inhibitory activity of curcumin on the anti-oxidant enzyme Thioredoxin Reductase-1 (TxnRd1) is required for curcumin-mediated radiosensitization of squamous carcinoma cells
ROS↑, induced reactive oxygen species
ERK↑, sustained ERK1/2 activation
Dose∅, Curcumin treatment resulted in a dose-dependent decrease in TxnRd activity with an IC50 of approximately 10 µM in both cell lines
cl‑PARP↑, curcumin induced a robust increase in cleaved PARP

475- CUR,    Curcumin induces apoptotic cell death in human pancreatic cancer cells via the miR-340/XIAP signaling pathway
- in-vitro, PC, PANC1
Apoptosis↑,
cl‑Casp3↑,
miR-340↑,
cl‑PARP↑,
XIAP↓,

477- CUR,    Curcumin induces G2/M arrest and triggers autophagy, ROS generation and cell senescence in cervical cancer cells
- in-vitro, Cerv, SiHa
TumCP↓,
TumCCA↑, Inducing G2/M cell cycle arrest
Apoptosis↑,
TumAuto↑,
CycB/CCNB1↓, cyclins B1
CDC25↓,
ROS↑,
p62↑,
LC3‑Ⅱ/LC3‑Ⅰ↑,
cl‑Casp3↑,
cl‑PARP↑,
P53↑,
P21↑,

132- CUR,    Targeting multiple pro-apoptotic signaling pathways with curcumin in prostate cancer cells
- in-vitro, Pca, PC3
TumCCA↑, inducing a chronic ER stress mediated cell death and activation of cell cycle arrest, UPR, autophagy and oxidative stress responses.
ROS↑, correlating with the upregulation of reactive oxygen species
TumAuto↑,
UPR↑, The upregulation of eIF2α in curcumin-treated cells, suggests activation of the UPR-associated PERK pathway
ER Stress↑,
Casp3↑, Chronic ER stress induction was concomitant with the upregulation of pro-apoptotic markers (caspases 3,9,12) and Poly (ADP-ribose) polymerase.
Casp9↑,
Casp12↑,
PARP↑,
other↝, Curcumin-treated PC3 cells expressed 146 upregulated and 184 downregulated proteins when compared with control PC3 cells (treated with DMSO).
GRP78/BiP↑, GRP78 and the PDI family were upregulated by 1.69 and ≥1.25-fold respectively
PDI↑,
eIF2α↑, other upregulated proteins related to ER stress figure eukaryotic translation initiation factor 2A (EIF2A), with a significant fold change of 1.25,
other↝, downregulated antioxidant markers such as peroxiredoxin 6 (PRDX6) and protein DJ-1 (PARK7) with significant fold changes of –1.39 and –1.51, respectively

136- CUR,  docx,    Combinatorial effect of curcumin with docetaxel modulates apoptotic and cell survival molecules in prostate cancer
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
Bcl-2↓, combined treatment with curcumin with docetaxel down-regulates the expression of the anti-apoptotic proteins BCL-2, BCL-XL and MCL-1 in DU145 and PC3 cells
Bcl-xL↓,
Mcl-1↓,
BAX↑, Whereas, the expression of the pro-apoptotic markers BAK and BID were significantly up-regulated in curcumin with docetaxel treated group compared to curcumin and docetaxel-treated group alone
BID↑,
PARP↑, combined treatment with curcumin and docetaxel in DU145 and PC3 cells enhanced proteolysis of PARP compared
NF-kB↓, Curcumin blocks NF-κB activation in docetaxel-treated PCa cells
CDK1↓, treatment of curcumin and docetaxel significantly reduced the expression of the proliferation marker CDK-1 and inflammatory marker COX-2
COX2↓,
RTK-RAS↓,
PI3K/Akt↓, combined treatment of curcumin and docetaxel reduced the expression of PI3K, phospho-AKT, EGFR and HER2 in both DU145 and PC3 cells
EGFR↓,
HER2/EBBR2↓, docetaxel in combination with curcumin down-regulates the expression of HER2 and EGFR resulting inhibition of the expression of PI3K kinase and phospho-AKT
P53↑,
ChemoSen↑, The combined treatment of curcumin and docetaxel inhibited the proliferation and induced apoptosis significantly higher than the curcumin and docetaxel-treated group alone.

152- CUR,    Anti-cancer activity of curcumin loaded nanoparticles in prostate cancer
- in-vivo, Pca, NA
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↓,

118- CUR,    Curcumin analog WZ35 induced cell death via ROS-dependent ER stress and G2/M cell cycle arrest in human prostate cancer cells
- in-vitro, Pca, PC3 - in-vitro, Pca, DU145
ROS↑, WZ35 treatment for 30 min significantly induced reactive oxygen species (ROS) production in PC-3 cells.
Bcl-2↓,
PARP↑,
cDC2↓, decreased expression of CDC2, cyclinB1, and MDM2
CycB/CCNB1↓,
MDM2↓,
eff↓, Co-treatment with the ROS scavenger NAC completely abrogated the induction of WZ35 on cell apoptosis,
eIF2α↑, WZ35 treatment also induced a constant increase in the level of phosphorylated eIF2α 3 to 12 h after WZ35 treatment
ATF4↑, ATF4 expression also increased in a similar manner with p-eIF2α
CHOP↑, CHOP protein expression apparently increased 9-24 h after WZ35 treatment and peaked at 12 h
ER Stress↑, results suggest that WZ35 can induce ER stress in prostate cancer cells
TumCCA↑, WZ35 induced cell cycle arrest in G2/M phase in PC-3 cells

831- GAR,  CUR,    Induction of apoptosis by garcinol and curcumin through cytochrome c release and activation of caspases in human leukemia HL-60 cells
- in-vitro, AML, HL-60
Apoptosis↑,
Casp3↑,
MMP↓, 20 microM caused a rapid loss of mitochondrial transmembrane potential
Cyt‑c↑, release of mitochondrial cytochrome c into cytosol
proCasp9↑,
Bcl-2↓,
BAX↑,
PARP↓, degradation of PARP
DNAdam↑,
DFF45↓, through the digestion of DFF-45

150- NRF,  CUR,  docx,    Subverting ER-Stress towards Apoptosis by Nelfinavir and Curcumin Coexposure Augments Docetaxel Efficacy in Castration Resistant Prostate Cancer Cells
- in-vitro, Pca, C4-2B
p‑Akt↓,
p‑eIF2α↑, phosphorylated
ER Stress↑, Acute exposure (3–9 hrs) to this 3-drug combination intensified ER-stress induced pro-apoptotic markers, i.e. ATF4, CHOP, and TRIB3.
ATF4↑, 3-drug combination rapidly enhances ER-stress associated death sensors, CHOP, ATF-4 and TRIB3 in C4-2B cells
CHOP↑,
TRIB3↑,
ChemoSen↑, subverting ER-stress towards apoptosis using adjuvant therapy with NFR and CUR can chemosensitize the CRPC cells to DTX therapy.
Casp3↑, NFR or CUR alone could increase Caspase-3 activity in DTX exposed cells
cl‑PARP↑, PARP cleavage assays further confirmed this differential effect of drug combination on apoptotic cell death. In C4-2B cells, a 9-fold increase was observed
BID↑, 3-drug combination rapidly increases ER-stress transducers, BiP, eIF2µ and Xbp-1 in C4-2B cells
XBP-1↑,


Showing Research Papers: 1 to 16 of 16

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 16

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Ferroptosis↑, 1,   GPx1↓, 1,   GPx4↓, 1,   ROS↑, 7,   TrxR↓, 1,  

Mitochondria & Bioenergetics ⓘ

CDC25↓, 1,   MMP↓, 2,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   PI3K/Akt↓, 1,  

Cell Death ⓘ

14-3-3 proteins↓, 1,   Akt↓, 3,   p‑Akt↓, 6,   Apoptosis↑, 7,   BAD↑, 1,   p‑BAD↓, 2,   BAX↑, 5,   Bcl-2↓, 6,   Bcl-xL↓, 3,   BID↑, 2,   BIM↑, 1,   Casp12↑, 1,   Casp3↑, 4,   cl‑Casp3↑, 4,   Casp9↑, 2,   cl‑Casp9↑, 1,   proCasp9↑, 1,   Cyt‑c↑, 1,   Ferroptosis↑, 1,   MAPK↓, 1,   Mcl-1↓, 2,   MDM2↓, 1,   PUMA↑, 1,   survivin↓, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,   RTK-RAS↓, 1,  

Transcription & Epigenetics ⓘ

miR-205↑, 1,   miR-21↓, 1,   other↝, 2,  

Protein Folding & ER Stress ⓘ

CHOP↑, 3,   eIF2α↑, 2,   p‑eIF2α↑, 2,   ER Stress↑, 3,   GRP78/BiP↑, 1,   HSP27↑, 1,   UPR↑, 1,   XBP-1↑, 1,  

Autophagy & Lysosomes ⓘ

ATG3↑, 2,   ATG5↑, 1,   Beclin-1↑, 3,   LC3‑Ⅱ/LC3‑Ⅰ↑, 2,   LC3I↓, 1,   LC3II↑, 1,   p62↓, 1,   p62↑, 2,   TumAuto↑, 4,  

DNA Damage & Repair ⓘ

DFF45↓, 1,   DNAdam↑, 1,   DNMT1↓, 1,   P53↑, 4,   p‑P53↑, 1,   PARP↓, 1,   PARP↑, 5,   p‑PARP↑, 1,   cl‑PARP↑, 9,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CycB/CCNB1↓, 2,   P21↑, 2,   TumCCA↓, 1,   TumCCA↑, 5,  

Proliferation, Differentiation & Cell State ⓘ

Axin2↑, 1,   cDC2↓, 1,   CSCs↓, 1,   ERK↑, 1,   p‑ERK↑, 1,   GSK‐3β↓, 1,   IGFR↓, 1,   mTOR↓, 1,   p‑mTOR↓, 2,   NOTCH↓, 2,   p‑P70S6K↓, 1,   PI3K↓, 2,   PTEN↑, 1,   Shh↓, 1,   STAT3↓, 3,   TumCG↓, 3,   Wnt↓, 2,  

Migration ⓘ

miR-340↑, 1,   TRIB3↑, 1,   TumCI↓, 2,   TumCP↓, 3,   TumMeta↓, 2,   β-catenin/ZEB1↓, 3,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   ATF4↑, 3,   ECM/TCF↓, 1,   EGFR↓, 2,   PDI↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   JAK↓, 1,   NF-kB↓, 3,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   ChemoSen↑, 4,   Dose∅, 1,   eff↓, 1,   Half-Life↓, 1,   RadioS↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   EGFR↓, 2,   HER2/EBBR2↓, 1,   TRIB3↑, 1,  
Total Targets: 113

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PARP, poly ADP-ribose polymerase (PARP) cleavage
16 Curcumin
2 Docetaxel
1 Radiotherapy/Radiation
1 Garcinol
1 nelfinavir/Viracept
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#:239  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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