Curcumin 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):

Suppression of NF-κB / STAT3 inflammatory-survival signaling, reducing cytokine, COX-2, iNOS, anti-apoptotic, invasion, and treatment-resistance programs.
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.
Mitochondrial injury and intrinsic apoptosis, including mitochondrial membrane potential loss, cytochrome-c release, caspase activation, PARP cleavage, and ER-stress/UPR involvement.
PI3K/AKT/mTOR and MAPK pathway modulation, contributing to growth arrest, autophagy modulation, apoptosis sensitization, and reduced survival signaling.
Wnt/β-catenin, Hedgehog/GLI, Notch, and cancer-stem-cell suppression, reducing stemness, EMT, invasion, and recurrence-associated phenotypes in models.
Hypoxia / HIF-1α and glycolysis inhibition, including reduced GLUT1, HK2, LDHA, PKM2, lactate/ECAR, and Warburg-like metabolic support in selected models.
Anti-angiogenic and anti-metastatic modulation, including VEGF, MMPs, uPA, CXCR4/SDF-1, TGF-β/α-SMA, FAK, and EMT-related axes.
Epigenetic and transcriptional reprogramming, including reported HDAC, DNMT, EZH2, Sp-family, p53, and microRNA-related effects.
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.
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">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

Scientific Papers found: Click to Expand⟱

4415-

AgNPs,

SDT,

CUR,

Examining the Impact of Sonodynamic Therapy With Ultrasound Wave in the Presence of Curcumin-Coated Silver Nanoparticles on the Apoptosis of MCF7 Breast Cancer Cells

in-vitro,

BC,

MCF-7

29.3 ± 5.6 nm

 48.23 µg/ml

SDT was performed using an US frequency of 1 MHz, intensity of 2 W/cm2, and a distance of 2 cm.

tumCV↓, Curcumin-coated silver nanoparticles (Cur@AgNPs) have shown potential as a sensitizer, demonstrating adverse effects on cancer cell survival.
BAX↑, proapoptotic genes, such as Bax and Caspase-3, increased, while the expression of the antiapoptotic gene Bcl-2 decreased in MCF7 cells treated with the SDT.
Casp3↑,
Bcl-2↓,
eff↑, effect of SDT in the presence of Cur@AgNPs decreases cell viability dependence on US mode
ROS↑, Combined treatment increased the amount of ROS induction
sonoS↑, Higher concentrations of AgNPs (100 μg/ml) acted as acoustic sensitizers and enhanced ROS production
eff↑, Using curcumin as a biological coating reduced the toxicity of AgNPs and improved their significant effects with SDT
MMP↓, reduction in mitochondrial membrane potential (MMP) and the opening of mitochondrial permeability transition pores (mPTPs)
Cyt‑c↑, ultimately facilitating the release of cytochrome c from the mitochondria into the cytosol.

3446-

ALA,

CUR,

The Potential Protective Effect of Curcumin and α-Lipoic Acid on N-(4-Hydroxyphenyl) Acetamide-induced Hepatotoxicity Through Downregulation of α-SMA and Collagen III Expression

in-vivo,

Nor,

Curc (200 mg/kg p. o.) and/or Lip acid (100 mg/kg i. p.)

rats

*hepatoP↑, Curc and Lip acid can be considered as promising natural therapies against liver injury, induced by NHPA, through their antioxidant and antifibrotic actions.
*α-SMA↓, Curc and Lip acid reduced the expression of alpha-smooth muscle actin and collagen III, upregulated by NHPA intoxication
*COL3A1↓,
*ROS↓, scavenging activity to ROS and a capacity to regenerate endogenous antioxidants such as GSH, and vitamins C and E.
*GSH↑,
*ALAT↓, ALT, AST, and ALP activity levels compared to those of the control group. The use of NACS, Curc, and/or Lip acid significantly reduced the toxic effects of NHPA on those enzymes,
*AST↓,
*ALP↓,
*MDA↓, The combination therapy showed an apparent reduction in MDA level more than other treatments

2635-

Api,

CUR,

Synergistic Effect of Apigenin and Curcumin on Apoptosis, Paraptosis and Autophagy-related Cell Death in HeLa Cells

in-vitro,

Cerv,

HeLa

TumCD↑, Treatment with a combination of apigenin and curcumin increased the expression levels of genes related to cell death in HeLa cells 1.29- to 27.6-fold.
eff↑, combination of curcumin and apigenin showed a synergistic anti-tumor effect
TumAuto↑, autophagic cell death, as well as ER stress-associated paraptosis
ER Stress↑,
Paraptosis↑,
GRP78/BiP↓, GRP78 expression was down-regulated, and massive cytoplasmic vacuolization was observed in HeLa cells
Dose↝, combined use of 0.09 μg/μl curcumin and 0.06 μg/μl apigenin showed a synergistic anti-tumor effect

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

147-

ATG,

EGCG,

CUR,

Increased chemopreventive effect by combining arctigenin, green tea polyphenol and curcumin in prostate and breast cancer cells

in-vitro,

Pca,

LNCaP

  5–10μM Cur, 1μM Arc and 40μM EGCG

in-vitro,

Pca,

MCF-7

  5–10μM Cur, 1μM Arc and 40μM EGCG

Bax:Bcl2↑, combination treatment significantly increased the ratio of Bax to Bcl-2 proteins, decreased the activation of NFκB, PI3K/Akt and Stat3
NF-kB↓, arctigenin demonstrated the strongest ability to inhibit the activation of both PI3K/Akt and NFκB pathways in both LNCaP and MCF-7 cells.
PI3K/Akt↓,
STAT3↓,
chemoPv↑, combining Arc and EGCG with Cur to enhance chemoprevention in both prostate and breast cancer.
TumCP↓, combining Arc and EGCG with Cur to enhance chemoprevention in both prostate and breast cancer.
TumCCA↑, EGCG significantly increased the effect of curcumin on cell cycle arrest at G0/G1 phase in MCF-7 cells, and the effect was further enhanced by the addition of arctigenin
TumCMig↓, EGCG and arctigenin alone or in combination with curcumin significantly decreased the number of migrated MCF-7 cells compared to control

2703-

BBR,

CUR,

SFN,

UA,

GamB

Naturally occurring anti-cancer agents targeting EZH2

Review,

Var,

EZH2↓, In fact, several natural products such as curcumin, triptolide, ursolic acid, sulforaphane, davidiin, tanshindiols, gambogic acid, berberine and Alcea rosea have been shown to serve as EZH2 modulators.

3754-

BBR,

CUR,

EGCG,

Hup,

Traditional Chinese medicinal herbs as potential AChE inhibitors for anti-Alzheimer’s disease: A review

*AChE↓, Berberine (9) has gained considerable attention due to its wide pharmacological potentials and several biological properties, such as acetylcholinesterase and butyrylcholinesterase inhibitory, antioxidant, monoamine oxidase oxidase,
*Aβ↓, amyloid-b peptide level-reducing, cholesterol- lowering and renoprotective activities
*LDL↓,
*RenoP↑,
*BChE↓,
*eff↑, Above all, the berberine-pyrocatechol hybrid (14) showed a strong AChE inhibitor activity (IC50 of 123 Â± 3 nM) [34]
*BACE↓, Curcumin: inhibite the rBACE1 activity [42]. In addition, it has made good inhibitory effect on acetylcholinesterase activity
*AChE↓, EGCG promoted brain health, prevented AD progression, and inhibited the AChE activity [52,53].
*eff↑, EGCG could enhance the effect of huperzine A on inhibiting AChE.

3514-

Bor,

CUR,

Effects of Curcumin and Boric Acid Against Neurodegenerative Damage Induced by Amyloid Beta

in-vivo,

AD,

rat

*DNAdam↓, Co-administration of BA and curcumin on synaptosomes exposed to Aβ1-42 resulted in a significant decrease in DNA fragmentation values, MDA levels, and AChE activities.
*MDA↓,
*AChE↓,
*neuroP↑, BA and curcumin had protective effects on rat brain synaptosomes against Aβ1-42 exposure.
*ROS↓, BA and curcumin treatment can have abilities to prevent the alterations of the cholinergic system and inhibit oxidative stress in the cerebral cortex synapses of Aβ1-42 exposed.
*NO↓, Synaptosomes treated with BA showed a significant reduction in MDA and NO levels

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↓,

145-

CA,

CUR,

The anti-cancer effects of carotenoids and other phytonutrients resides in their combined activity

in-vitro,

Pca,

LNCaP

in-vitro,

Pca,

PC3

in-vitro,

PC,

DU145

AR↓, Phytonutrients synergistically inhibit androgen signaling
ARE/EpRE↑, x4 the sum of single ingredients
TumCP↓, Phytonutrients inhibit prostate cancer cell proliferation
PSA↓, combination of three compounds such as in the case of curcumin, vitamin E and the tomato extract showed a stronger synergistic effect than each pair of compounds. The inhibition of PSA secretion

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

5953-

Cela,

CUR,

The Combination of Celastrol and Curcumin Enhances the Antitumor Effect in Nasopharyngeal Carcinoma by Inducing Ferroptosis

vitro+vivo,

NPC,

eff↑, The results indicated that low doses of celastrol (0.7 μM) alone do not inhibit proliferation in NPC cells. However, when combined with curcumin, there is a significant enhancement of the antiproliferative effect.
TumCP↓,
GPx4↓, while notably decreasing solute carrier family 7 member 11 and glutathione peroxidase 4,
eff↑, combined treatment exhibited significant antitumor efficacy with low toxic side effects in a xenograft model.
TumAuto↑, Combined Treatment with Curcumin and Low-Dose Celastrol Induced Autophagy in the CNE1 Cell Line
Ferroptosis↑, Ferroptosis Plays a Critical Role in Low-Dose Celastrol Plus Curcumin-Induced Cell Death
Dose↝, more significant decrease observed in cells treated with 0.7 μM celastrol combined with 35 μM curcumin
ACSL4↑, Only the combination of 0.7 μM celastrol and 35 μM curcumin led to a significant increase in ACSL4 levels
toxicity↓, The Combination of Celastrol and Curcumin Demonstrates a Significant Tumor-Suppressive Effect with Low Toxicity

6027-

CGA,

CUR,

EGCG,

QC,

RES

Contribution of Non-Coding RNAs to Anticancer Effects of Dietary Polyphenols: Chlorogenic Acid, Curcumin, Epigallocatechin-3-Gallate, Genistein, Quercetin and Resveratrol

Review,

Nor,

*ROS↓, polyphenols have similar chemical and biological properties in that they can act as antioxidants and exert the anticancer effects via cell signaling pathways involving their reactive oxygen species (ROS)-scavenging activity.
ROS↑, These polyphenols may also act as pro-oxidants under certain conditions, especially at high concentrations.

5995-

Chit,

CUR,

Enhancement of anticancer activity and drug delivery of chitosan-curcumin nanoparticle via molecular docking and simulation analysis

vitro+vivo,

Var,

eff↑, Formulated CSCur NPs were assessed for in-vitro release, which exhibited a sustained release pattern and four-fold higher cytotoxic activity in a nanoparticulated system.
EPR↑, Enhanced uptake, apoptotic effect of CSCur NPs were established by morphological changes in cells as observed by fluorescence microscopy and FE-SEM.
DNAdam↑, DNA damage, cell-cycle blockage and elevated ROS levels further confirm the anticancer activity of the CSCur NPs following apoptotic pathways.
TumCCA↑,
ROS↑,
toxicity↓, In-vivo study on Danio rerio, for uptake and toxicity reveal the particle's biocompatibility and nontoxicity

428-

Chit,

docx,

CUR,

Chitosan-based nanoparticle co-delivery of docetaxel and curcumin ameliorates anti-tumor chemoimmunotherapy in lung cancer

vitro+vivo,

Lung,

H460

4, 8, 12, 16, 20, 24 and 28 μg/mL, 24 h; 5 mg/kg, 24 h

vitro+vivo,

Lung,

H1299

vitro+vivo,

Lung,

A549

vitro+vivo,

Lung,

PC9

MDSCs↓,
TregCell↓,
IL10↓,
NK cell↑,

5792-

CRMs,

HCA,

CUR,

EGCG,

GAR

Caloric restriction mimetics: natural/physiological pharmacological autophagy inducers

Review,

Nor,

*CRM↓, AcCoA depleting agents (e.g., hydroxycitrate),
*Dose?, acetyltransferase inhibitors (e.g., anacardic acid, curcumin, epigallocatechin-3-gallate, garcinol, spermidine)
*AntiAge↑, Another common characteristic of these agents is their capacity to reduce aging-associated diseases and to confer protective responses against ischemia-induced organ damage.
*Acetyl-CoA↓, Altogether, these observations point to the idea that starvation causes autophagy because it results in the early depletion of AcCoA
*SIRT1↑, nduction of the deacetylase activity of sirtuins (as a result of changing NADH/NAD+ ratios and increased SIRT1 expression)
*AMPK↑, activation of AMPK activity (as a result of changing ATP/ADP ratios)
*mTORC1↓, inhibition of MTORC1 (as a result of amino acid depletion).
*AntiAge↑, CR or intermittent fasting are known for their wide life-span-extending
chemoP↑, fasting can reduce the subjective and objective toxicity of cytotoxic anticancer chemotherapies, both in humans and in mouse models, at the same time that it improves treatment outcome in mice

3628-

Cro,

VitE,

CUR,

Vitamin E, Turmeric and Saffron in Treatment of Alzheimer’s Disease

Review,

AD,

*antiOx↑, Vitamin E is a potent antioxidant that may have beneficial effects in Alzheimer’s in dealing with oxidative stress
*ROS↓,
*lipid-P↓, Alpha-tocopherol was found as protective against lipid peroxidation
*Aβ↓, Researchers found that all forms of tocopherol enhanced the Aβ production and decreased the Aβ degradation. T
*AChE↓, vitamin E treatment significantly restored acetylcholinesterase activity and increased the Na+/K+ ATPase activity.
*cognitive↑, Although high plasma vitamin E is linked to better cognitive performance [
*Inflam↓, curcumin is effective in AD as an antioxidant, anti-inflammatory therapeutic agent that improves the cognitive functions

4826-

CUR,

The Bright Side of Curcumin: A Narrative Review of Its Therapeutic Potential in Cancer Management

Review,

Var,

*antiOx↑, Curcumin demonstrates strong antioxidant and anti-inflammatory properties, contributing to its ability to neutralize free radicals and inhibit inflammatory mediators
*Inflam↑,
*ROS↓,
Apoptosis↑, Its anticancer effects are mediated by inducing apoptosis, inhibiting cell proliferation, and interfering with tumor growth pathways in various colon, pancreatic, and breast cancers
TumCP↓,
BioAv↓, application is limited by its poor bioavailability due to its rapid metabolism and low absorption.
Half-Life↓,
eff↑, curcumin-loaded hydrogels and nanoparticles, have shown promise in improving curcumin bioavailability and therapeutic efficacy.
TumCCA↑, Studies have demonstrated that curcumin can suppress the proliferation of cancer cells by interfering with the cell cycle [21,22]
BAX↑, Curcumin enhances the expression of pro-apoptotic proteins such as Bax, Bak, PUMA, Bim, and Noxa and death receptors such as TRAIL-R1/DR4 and TRAIL-R2/DR5
Bak↑,
PUMA↑,
BIM↑,
NOXA↑,
TRAIL↑,
Bcl-2↓, curcumin decreases the levels of anti-apoptotic proteins like Bcl-2, Bcl-XL, survin, and XIAP
Bcl-xL↓,
survivin↓,
XIAP↓,
cMyc↓, This shift in the balance of apoptotic regulators facilitates the release of cytochrome c from mitochondria [33,35] and activates caspases
Casp↑,
NF-kB↓, Curcumin suppresses the activity of key transcription factors like NF-κB, STAT3, and AP-1 and interferes with critical signal transduction pathways such as PI3K/Akt/mTOR and MAPK/ERK.
STAT3↓,
AP-1↓,
angioG↓, curcumin inhibits angiogenesis and metastasis by downregulating VEGF, VEGFR2, and matrix metalloproteinases (MMPs).
TumMeta↑,
VEGF↓,
MMPs↓,
DNMTs↓, Epigenetic modifications through the inhibition of DNA methyltransferases (DNMTs) and histone deacetylases (HDACs) further contribute to its anticancer properties.
HDAC↓,
ROS↑, curcumin-loaded nanoparticles showed significant cytotoxicity in the SCC25, MDA-MB-231, and A549 cell lines, with a decrease in tumor cell proliferation, an increase in ROS, and an increase in apoptosis.

4831-

CUR,

The dual role of curcumin and ferulic acid in counteracting chemoresistance and cisplatin-induced ototoxicity

in-vitro,

NA,

*NRF2↑, We reported that both polyphenols show antioxidant and oto-protective activity in the cochlea by up-regulating Nrf-2/HO-1 pathway and downregulating p53 phosphorylation.
*P53↓,
*NF-kB↓, only curcumin is able to influence inflammatory pathways counteracting NF-κB activation
ROS↑, In human cancer cells, curcumin converts the anti-oxidant effect into a pro-oxidant and anti-inflammatory one
Inflam↓,
ChemoSen↑, Curcumin exerts permissive and chemosensitive properties by targeting the cisplatin chemoresistant factors Nrf-2, NF-κB and STAT-3 phosphorylation.

4710-

CUR,

Curcumin inhibits migration and invasion of non-small cell lung cancer cells through up-regulation of miR-206 and suppression of PI3K/AKT/mTOR signaling pathway

in-vitro,

Lung,

A549

TumCMig↓, Curcumin significantly inhibited migration and invasion in A549 cells, accompanied by significantly elevated miR-206 expression.
TumCI↓,
miR-206↑, Overexpression of miR-206 could inhibit migration and invasion of A549 cells, but it could also significantly decrease the phosphorylation levels of mTOR and AKT.
p‑mTOR↓,
p‑Akt↓,

4709-

CUR,

Curcumin Regulates Cancer Progression: Focus on ncRNAs and Molecular Signaling Pathways

Review,

Var,

miR-21↓, Curcumin can effectively repress the miR-21/PTEN/Akt molecular pathway to inhibit cell proliferation and induce apoptosis in gastric cancer cells
TumCP↓, Curcumin can inhibit the proliferation, migration, invasion and promote apoptosis of retinoblastoma cells, which function through up-regulating the miR-99a expression and then inhibiting JAK/STAT signaling pathway
TumCMig↓,
TumCI↓,
Apoptosis↑,
miR-99↑,
JAK↓,
STAT↓,
cycD1/CCND1↓, curcumin can suppress the cell proliferation by down-regulations of cyclinD1 and up-regulations of p21 expression.
P21↑,
ChemoSen↑, curcumin combined with chemotherapy drugs may play a better therapeutic effect via JAK/STAT signaling pathway
miR-192-5p↑, curcumin enhanced the expression level of miR−192−5p and decreased the expression of c−Myc.
cMyc↓,
Wnt↓, curcumin suppresses colon cancer by inhibiting Wnt/β-catenin pathway via down-regulating miR-130a
β-catenin/ZEB1↓,
miR-130a↓,

4708-

CUR,

Molecular mechanisms underlying curcumin-mediated microRNA regulation in carcinogenesis; Focused on gastrointestinal cancers

Review,

GC,

chemoPv↑, Curcumin is well known for its chemopreventive and anti-cancer properties.
AntiCan↑,
*antiOx↑, Mechanistically, curcumin exerts its biological impacts via antioxidant and anti-inflammatory effects through the interaction with various transcription factors and signaling molecules.
*Inflam↓,
miR-21↓, Table 1
miR-34a↑,
miR-200b↑,
miR-27a-3p↓,

4707-

CUR,

The Potential Role of Curcumin as a Regulator of microRNA in Colorectal Cancer: A Systematic Review

Review,

Var,

miR-497↑, Curcumin was found to cause the upregulation of miR-497, miR-200c, miR-200b, miR-409-3p, miR‐34, miR‐126, miR-145, miR-206, miR-491, miR-141, miR-429, miR-101, and miR-15a
miR-200c↑,
miR-409-3p↑,
miR-34a↑,
miR-126↑,
miR-145↑,
miR-206↑,
miR-491↑,
miR-141↑,
miR-429↑,
miR-101↑,
miR-15↑,
miR-21↓, and the downregulation of miR-21, miR-155, miR‐221, miR‐222, miR-17-5p, miR-130a, miR-27, and miR-20a.
miR-155↓,
miR-221↓,
miR‐222↓,
miR-17↓,
miR-130a↓,
miR-27a-3p↓,
miR-20↓,

4828-

CUR,

Role of pro-oxidants and antioxidants in the anti-inflammatory and apoptotic effects of curcumin (diferuloylmethane)

Review,

Var,

*NF-kB↓, TNF-mediated NF-κB activation was inhibited by curcumin
ROS↑, curcumin induced the production of reactive oxygen species and modulated intracellular GSH levels.

4829-

CUR,

Dual Action of Curcumin as an Anti- and Pro-Oxidant from a Biophysical Perspective

Review,

Var,

*antiOx↑, therapeutic effects against different disorders, mostly due to its anti-oxidant properties.
ROS↑, However, curcumin can act as a pro-oxidant when blue light is applied, since upon illumination it can generate singlet oxygen
*lipid-P↓, In addition to inhibiting lipid peroxidation, curcumin appears to reduce induciblenitric oxide (NO) synthase (iNOS) activity.
*iNOS↓,
*BioAv↓, poor bioavailability is the key to curcumin’s health-promoting effects,

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

4675-

CUR,

Curcumin improves the efficacy of cisplatin by targeting cancer stem-like cells through p21 and cyclin D1-mediated tumour cell inhibition in non-small cell lung cancer cell lines

in-vitro,

NSCLC,

A549

10–40 µM

ChemoSen↑, we showed that curcumin enhanced the sensitivity of the double-positive (CD166+/EpCAM+) CSC subpopulation in non-small cell lung cancer (NSCLC) cell lines (A549 and H2170) to cisplatin-induced apoptosis and inhibition of metastasis.
CSCs↓, Curcumin enhances the sensitivity of the CSC subpopulation of CD166+/EpCAM+ cells to cisplatin-induced apoptosis
EpCAM↓, curcumin enhanced the inhibitory effects of cisplatin on the highly migratory CD166+/EpCAM+ subpopulation
TumCCA↓, combined treatments induced cell cycle arrest, therefore triggering CSC growth inhibition via the intrinsic apoptotic pathway.
VEGF↓, curcumin markedly decreased the metastasis of breast tumour cells to the lung and suppressed the expression of vascular endothelial growth factor (VEGF), matrix metalloproteinase-9 (MMP-9)
MMP9↓,
toxicity↓, Furthermore, curcumin has been found to be safe when administered at ≤10 g/day in humans

4881-

CUR,

SFN,

RES,

EGCG,

Lyco

An update of Nrf2 activators and inhibitors in cancer prevention/promotion

Review,

Var,

*NRF2↑, natural Nrf2 activators include curcumin, sulforaphane (SF), kahweol, resveratrol, garlic oganosulfur compounds, zerumbone, epigallocatechin-3-gallate, carnosol, cinnamonyl-based compounds, lycopene, and cafestol
*antiOx↑, these chemopreventive agents can activate the antioxidants, phase II detoxification factors, and transducers, and protect the cells from carcinogenic exposure

5229-

CUR,

Activation of Transcription Factor NF-κB Is Suppressed by Curcumin (Diferuloylmethane)

in-vitro,

Melanoma,

human myeloid ML-1a cells

NF-kB↓, Besides TNF, curcumin also blocked phorbol ester- and hydrogen peroxide-mediated activation of NF-κB.

4654-

CUR,

Stem Cell Therapy: Curcumin Does the Trick

Review,

Var,

*antiOx↑, Curcumin is a dietary polyphenol and a bioactive phytochemical agent that possesses anti-inflammatory, antioxidant, anticancer, and chemopreventive properties.
*Inflam↓,
AntiCan↑,
chemoPv↑,
*AntiAge↑, antiaging, and neuroprotective as well as wound healing and regenerative effects of curcumin.
*neuroP↑,
*Wound Healing↑,

4171-

CUR,

Curcumin produces neuroprotective effects via activating brain-derived neurotrophic factor/TrkB-dependent MAPK and PI-3K cascades in rodent cortical neurons

in-vivo,

NA,

rodent

*BDNF↑, treatment of curcumin increased BDNF and phosphor-TrkB
*TrkB↑,
*CREB↑, curcumin-induced increase in phosphorylated cyclic AMP response element binding protein (CREB), which has been implicated as a possible mediator of antidepressant actions
*Mood↑,
*neuroP↑, Therefore, we hypothesize the neuroprotection of curcumin might be mediated via BDNF/TrkB-MAPK/PI-3K-CREB signaling pathway.

4175-

CUR,

Effects of curcumin on learning and memory deficits, BDNF, and ERK protein expression in rats exposed to chronic unpredictable stress

in-vivo,

NA,

CUS rats

*BDNF↑, CUS reduced hippocampal BDNF and ERK levels, while curcumin effectively reversed these alterations
*ERK↑, related to its aptitude to promote BDNF and ERK in the hippocampus.

4176-

CUR,

Effects of curcumin (Curcuma longa) on learning and spatial memory as well as cell proliferation and neuroblast differentiation in adult and aged mice by upregulating brain-derived neurotrophic factor and CREB signaling

in-vivo,

AD,

Aged mice

*BDNF↑, Upregulating Brain-Derived Neurotrophic Factor and CREB Signaling
*CREB↑,

4337-

CUR,

Inhibitory effect of curcumin, a food spice from turmeric, on platelet-activating factor- and arachidonic acid-mediated platelet aggregation through inhibition of thromboxane formation and Ca2+ signaling

in-vitro,

NA,

*AntiAg↑, We show that curcumin inhibited platelet aggregation mediated by the platelet agonists epinephrine (200 μM), ADP (4 μM), platelet-activating factor (PAF; 800 nM), collagen (20 μg/mL), and arachidonic acid (AA: 0.75 mM).
*TXA2↓, results suggest that the curcumin-mediated preferential inhibition of PAF- and AA-induced platelet aggregation involves inhibitory effects on TXA2 synthesis and Ca2+ signaling, but without the involvement of PKC.

4650-

CUR,

Curcumin and cancer stem cells: curcumin has asymmetrical effects on cancer and normal stem cells

Review,

Var,

SCD1↓, Curcumin has been shown to have numerous cytotoxic effects on cancer stem cells (CSCs).
IL6↓, This is due to its suppression of the release of cytokines, particularly interleukin (IL)-6, IL-8 and IL-1
IL8↓,
IL1↓,
*selectivity↑, curcumin has little toxicity against normal stem cells (NSCs).
Wnt↝, effects at multiple sites along CSC pathways, such as Wnt, Notch, Hedgehog and FAK.
NOTCH↝,
HH↝,
FAK↝,

4651-

CUR,

Targeting cancer stem cells by curcumin and clinical applications

Review,

Var,

CSCs↓, recent research has shown that curcumin can target cancer stem cells (CSCs)
*toxicity↓, safety and tolerability of curcumin have been well-established by numerous clinical studies
*BioAv↝, Importantly, the low bioavailability of curcumin has been dramatically improved through the use of structural analogues or special formulations.
chemoP↑, promising agent in cancer chemoprevention and therapy

4652-

CUR,

Anticancer effect of curcumin on breast cancer and stem cells

Review,

BC,

TumCP↓, inhibiting cancer cell proliferation and metastasis and by inducing cell cycle arrest and apoptosis.
TumMeta↓,
TumCCA↑,
Apoptosis↑,
CSCs↓, curcumin inhibits the proliferation of breast cancer stem cells (BCSC), an important factor that influences cancer recurrence.
NF-kB↓, curcumin exhibited a potent antiproliferation effect by inhibiting the binding activity of NF-KB
Telomerase↓, Curcumin inhibited telomerase activity in human leukemia cells [21,22] and brain tumor cells [23] in a dose-dependent and time-dependent manner.
Cyt‑c↑, curcumin releases cytochrome C and upregulates caspase-9 and caspase-3 expression
Casp9↑,
Casp3↑,
E-cadherin↑, Curcumin inhibits the migratory ability of BSCS by amplifying the E-cadherin/β-catenin negative feedback loop.

4653-

CUR,

Curcumin: a promising agent targeting cancer stem cells

Review,

Var,

CSCs↓, evidence suggested that the dietary agent curcumin exerted its anti-cancer activities via targeting cancer stem cells of various origins such as those of colorectal cancer, pancreatic cancer, breast cancer, brain cancer, and head and neck cancer.

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.

4655-

CUR,

Inhibition of Cancer Stem-like Cells by Curcumin and Other Polyphenol Derivatives in MDA-MB-231 TNBC Cells

in-vitro,

BC,

CSCs↓, Curcumin, a polyphenol derived from turmeric (Curcuma longa), exhibits anticancer effects against breast cancer cells and BCSCs.
*BioAv↓, curcumin derivatives has been suggested as an approach to overcome the bioavailability and solubility problems of curcumin in humans, thereby increasing its anticancer effects

4656-

CUR,

EGCG,

Curcumin and epigallocatechin gallate inhibit the cancer stem cell phenotype via down-regulation of STAT3-NFκB signaling

in-vitro,

BC,

MDA-MB-231

 curcumin (10 μM) with/without EGCG (10 μM) for 48 hours.

in-vitro,

BC,

MCF-7

CSCs↓, Combined curcumin and EGCG treatment reduced the cancer stem-like Cluster of differentiation 44 (CD44) positive cell population.
CD44↓,
p‑STAT3↓, curcumin and EGCG specifically inhibited STAT3 phosphorylation and STAT3-NFkB interaction was retained.
NF-kB↓, Notably, curcumin is a potent inhibitor of NFκB
TumCI↓, Wound-healing assay revealed that curcumin and EGCG suppress cell invasiveness

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↓,

4672-

CUR,

An old spice with new tricks: Curcumin targets adenoma and colorectal cancer stem-like cells associated with poor survival outcomes

vitro+vivo,

CRC,

HCT116

CSCs↓, Curcumin targets proliferating stem cells in human colorectal adenoma models, with activity across all molecular subtypes.
Nanog↓, Evidence suggests these effects involve direct protein binding of curcumin to NANOG, a master regulator of CRC CSCs
BioAv↓, It is well established that curcumin has poor bioavailability, but appreciable concentrations can be detected in gastrointestinal tissue when it is taken orally in its standard form

4673-

CUR,

Curcumin and colorectal cancer: An update and current perspective on this natural medicine

Review,

CRC,

AntiCan↑, past few decades have overwhelmingly shown that curcumin exhibits a multitude of anti-cancer activities
GutMicro↝, Curcumin as a modulator of gut microbial environment

4674-

CUR,

Curcumin Shows Promise in Targeting Colorectal Cancer Stem-like Cells: Mechanistic Insights and Clinical Implications

Review,

CRC,

CSCs↓, Curcumin Suppresses CSCs and Tumor Formation In Vivo
Nanog↓, Mechanistic studies reveal curcumin binds to and inhibits NANOG, a key CSC regulator.

3862-

CUR,

RES,

The metalloproteinase ADAM10: A useful therapeutic target?

Review,

AD,

*SIRT1↑, Therefore, the Sirt1 activators curcumin and resveratrol are tested for their clinical impact on ADAM10 expression in AD.
*ADAM10↑,

6218-

CUR,

Exploring the Thioredoxin System as a Therapeutic Target in Cancer: Mechanisms and Implications

Review,

Var,

NF-kB↓, curcumin inhibits, among others, NF-κB and TrxR [177].
TrxR↓,
ROS↑, Several studies show that curcumin leads to an accumulation of ROS in tumor cells, inhibiting metastasis formation and inducing cell death and/or sensitizing the cells to radiation
TumMeta↓,
TumCD↑,
RadioS↑,
BioAv↝, Curcumin exhibits limitations for potential clinical applications due to its poor water solubility. Therefore, analogues have been developed, such as WZ26, which inhibits TrxR and restricts the proliferation and survival of tumor cells
BioAv↑, Phase I trial with theracurmin, a curcumin derivative that demonstrates higher bioavailability than curcumin, it was shown that a combination with irinotecan is safe and well-tolerated in patients with advanced solid tumors

6409-

CUR,

Curcumin prevents cisplatin-induced renal alterations in mitochondrial bioenergetics and dynamic

in-vivo,

Nor,

*FIS1↓, curcumin prevented the increase of mitochondrial fission 1 protein (FIS1), the decrease of optic atrophy 1 protein (OPA1) and the decrease of NAD+-dependent deacetylase sirtuin-3 (SIRT3)
*SIRT3↑,
*PTEN↓, as well as the increase in the mitophagy associated proteins parkin and phosphatase and tensin homologue (PTEN)-induced putative kinase protein 1 (PINK1).
*chemoP↑, In conclusion, the protective effect of curcumin in cisplatin-induced AKI

6408-

CUR,

Protective Effects of a Natural Product, Curcumin, against Amyloid β Induced Mitochondrial and Synaptic Toxicities in Alzheimer'S Disease

in-vitro,

AD,

SH-SY5Y

*mtDam↓, Mitochondrial function and cell viability were elevated in curcumin treated cells.
*eff↓,
*eff↑, Further, the protective effects of curcumin were stronger in pretreated SHSY5Y cells than in post-treated cells, indicating that curcumin works better in prevention than treatment in AD-like neurons.
*FIS1↓, significantly increased in Drp1, by 2.0 fold (p=0.004), and in Fis1, by 2.1 fold (
*lipid-P↓, lipid peroxidation were found ( p=0.002) in Aβ treated relative to untreated cells (figure 4). However, sig- nificantly decreased levels were found in the curcumin treated cells ( p=0.02) relative to untreated cells.
*ATP↑, Significantly increased levels of ATP were found in cells treated with curcumin

6232-

CUR,

Rad,

Chemo,

The Effectiveness of Curcumin in Treating Oral Mucositis Related to Radiation and Chemotherapy: A Systematic Review

Review,

Var,

*VEGF↑, Curcumin has been observed to stimulate vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF), both of which are responsible for cell proliferation and activity, thus promoting faster tissue healing
*Wound Healing↓,
*NRF2↑, Curcumin activates Nrf2 and promotes the release of antioxidant enzymes such as SOD, catalase (CAT), glutathione (GSH), and GSH-px
*Catalase↑,
*SOD↑,
*GSH↑,
*ROS↓, curcumin possesses powerful antioxidant properties that enable it to neu- tralize ROS, reducing oxidative damage to mucosal cells

Showing Research Papers: 1 to 50 of 331
Page 1 of 7 GPx&page=2&exSp=open">Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 331

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

NA, unassigned ⓘ

FIS1↓, 2,

Redox & Oxidative Stress ⓘ

antiOx↑, 6, Catalase↑, 1, GSH↑, 2, lipid-P↓, 3, MDA↓, 2, NRF2↑, 3, ROS↓, 6, SIRT3↑, 1, SOD↑, 1,

Mitochondria & Bioenergetics ⓘ

ATP↑, 1, mtDam↓, 1,

Core Metabolism/Glycolysis ⓘ

Acetyl-CoA↓, 1, ALAT↓, 1, AMPK↑, 1, CREB↑, 2, CRM↓, 1, LDL↓, 1, SIRT1↑, 2,

Cell Death ⓘ

iNOS↓, 1,

DNA Damage & Repair ⓘ

DNAdam↓, 1, P53↓, 1,

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1, mTORC1↓, 1, PTEN↓, 1,

Migration ⓘ

AntiAg↑, 1, COL3A1↓, 1, α-SMA↓, 1,

Angiogenesis & Vasculature ⓘ

NO↓, 1, TXA2↓, 1, VEGF↑, 1,

Immune & Inflammatory Signaling ⓘ

Inflam↓, 3, Inflam↑, 1, NF-kB↓, 2,

Synaptic & Neurotransmission ⓘ

AChE↓, 4, ADAM10↑, 1, BChE↓, 1, BDNF↑, 3, TrkB↑, 1,

Protein Aggregation ⓘ

Aβ↓, 2, BACE↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 2, BioAv↝, 1, Dose?, 1, eff↓, 1, eff↑, 3, selectivity↑, 1,

Clinical Biomarkers ⓘ

ALAT↓, 1, ALP↓, 1, AST↓, 1,

Functional Outcomes ⓘ

AntiAge↑, 3, chemoP↑, 1, cognitive↑, 1, hepatoP↑, 1, Mood↑, 1, neuroP↑, 3, RenoP↑, 1, toxicity↓, 1, Wound Healing↓, 1, Wound Healing↑, 1,
Total Targets: 60

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

Curcumin Cancer Research Results

Curcumin Cancer Mechanism Ranking

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned ⓘ

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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