Curcumin / HO-1 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
HO-1, HMOX1: Click to Expand ⟱
Source:
Type:
(Also known as Hsp32 and HMOX1)
HO-1 is the common abbreviation for the protein (heme oxygenase‑1) produced by the HMOX1 gene.
HO-1 is an enzyme that plays a crucial role in various cellular processes, including the breakdown of heme, a toxic molecule. Research has shown that HO-1 is involved in the development and progression of cancer.
-widely regarded as having antioxidant and cytoprotective effects
-The overall activity of HO‑1 helps to reduce the pro‐oxidant load (by degrading free heme, a pro‑oxidant) and to generate molecules (like bilirubin) that can protect cells from oxidative damage

Studies have found that HO-1 is overexpressed in various types of cancer, including lung, breast, colon, and prostate cancer. The overexpression of HO-1 in cancer cells can contribute to their survival and proliferation by:
  Reducing oxidative stress and inflammation
  Promoting angiogenesis (the formation of new blood vessels)
  Inhibiting apoptosis (programmed cell death)
  Enhancing cell migration and invasion
When HO-1 is at a normal level, it mainly exerts an antioxidant effect, and when it is excessively elevated, it causes an accumulation of iron ions.

A proper cellular level of HMOX1 plays an antioxidative function to protect cells from ROS toxicity. However, its overexpression has pro-oxidant effects to induce ferroptosis of cells, which is dependent on intracellular iron accumulation and increased ROS content upon excessive activation of HMOX1.

-Curcumin   Activates the Nrf2 pathway leading to HO‑1 induction; known for its anti‑inflammatory and antioxidant effects.
-Resveratrol  Induces HO‑1 via activation of SIRT1/Nrf2 signaling; exhibits antioxidant and cardioprotective properties.
-Quercetin   Activates Nrf2 and related antioxidant pathways; contributes to anti‑oxidative and anti‑inflammatory responses.
-EGCG     Promotes HO‑1 expression through activation of the Nrf2/ARE pathway; also exhibits anti‑inflammatory and anticancer properties.
-Sulforaphane One of the most potent natural HO‑1 inducers; triggers Nrf2 nuclear translocation and upregulates a battery of phase II detoxifying enzymes.
-Luteolin    Induces HO‑1 via Nrf2 activation; may also exert anti‑inflammatory and neuroprotective effects in various cell models.
-Apigenin   Has been reported to induce HO‑1 expression partly via the MAPK and Nrf2 pathways; also known for anti‑inflammatory and anticancer activities.
Scientific Papers found: Click to Expand⟱
6225- CUR,    Natural products for enhancing the sensitivity or decreasing the adverse effects of anticancer drugs through regulating the redox balance
- Review, Var, NA
ox-Trx1↑, TrxR1↓, TrxR↓, ROS↑, GSH/GSSG↓, eff↓, Fenton↑, H2O2↑, *NRF2↑, *Keap1↓, *HO-1↑, *NQO1↑, ChemoSen↑,
6223- CUR,    Curcumin Rewires the Tumor Metabolic Landscape: Mechanisms and Clinical Prospects
- Review, Var, NA
Ferroptosis↑, GutMicro↑, Akt↓, mTOR↓, NF-kB↓, Wnt↓, β-catenin/ZEB1↓, STAT3↓, TumCP↓, TumCI↓, TumMeta↓, AMPK↑, P53↑, NRF2↑, TumCCA↑, Apoptosis↑, Casp↑, GPx4↓, DNMTs↓, HDAC↓, VEGF↓, Imm↑, NK cell↑, Warburg↓, Hif1a↓, HK2↓, PKM2↓, LDHA↓, GLUT1↓, MCT1↓, AMPK↑, FASN↓, SCD1↓, GLS↓, Apoptosis↑, ETC↓, MMP↓, ROS↑, lipid-P↑, ChemoSen↑, PDK1↓, Beclin-1↓, ATP↓, Glycolysis↓, GlucoseCon↓, lactateProd↑, MMPs↓, GSH↓, G6PD↓, OXPHOS↓, SREBP2↓, COX2↓, AP-1↓, NADH↓, NRF2↑, HO-1↑, Iron↑, MDA↑, *ROS↓, *Inflam↓,
6216- CUR,    Role of Turmeric and Curcumin in Prevention and Treatment of Chronic Diseases: Lessons Learned from Clinical Trials
- Review, Var, NA
TumCG↓, angioG↓, EMT↓, TumCI↓, TumMeta↓, *GutMicro↑, *BioAv↓, *HO-1↑, *ROS↓, *COX2↓, *iNOS↓, PKCδ↓, EGFR↓, NF-kB↓, cJun↓, cFos↓, cMyc↓, Akt↓, PI3K↓, CDK4↓, *TNF-α↓, *CRP↓, *IL6↓, MMP9↓, VEGF↓, JAK↓, STAT↓, IL1↓, IL2↓, IL6↓, IL8↓, IL12↓, MCP1↓, Apoptosis↑, ER Stress↑, 5LO↓, XO↓, *NRF2↑, *HO-1↑, *AChE↓, *neuroP↑, *glucose↓, *GLUT2↑, *GLUT3↑, *GLUT4↑, *GlucoseCon↑, *AMPK↑, *BMD↑, *MDA↓, *eff↑, eff↑, P53↑, BAX↑, DNAdam↑, Bcl-2↓, CSCs↓, ALDH↓, CD133↑,
6215- CUR,    Curcumin: biochemistry, pharmacology, advanced drug delivery systems, and its epigenetic role in combating cancer
- Review, Var, NA
*antiOx↑, *Inflam↓, *BioAv↓, NF-kB↓, PI3K↓, Akt↓, Wnt↓, β-catenin/ZEB1↓, DNMTs↓, TumCI↓, TumMeta↓, *BioAv↑, *BioAv↑, angioG↓, VEGF↓, MMPs↓, *ROS↓, *SOD↑, *Catalase↑, *GSTs↑, *HO-1↑, *NRF2↑, mTOR↓, GSK‐3β↓, FOXO1↓, *radioP↑, *IL1↓, *IL6↓, *TNF-α↓, HATs↓, HDAC↓, ROS↑, ROS↑, MMP↓, Casp↑, Cyt‑c↑, COX1↓, COX2↓, PGE2↓, *cytoP450↓, ChemoSen↑, cardioP↑, eff↑,
6210- CUR,    Potential Roles and Mechanisms of Curcumin and its Derivatives in the Regulation of Ferroptosis
Ferroptosis↑, *Ferroptosis↓, ROS↑, Fenton↑, *IronCh↑, GPx4↓, MDA↑, GSH↓, *NRF2↑, *HO-1↑,
2819- CUR,  Chemo,    Curcumin as a hepatoprotective agent against chemotherapy-induced liver injury
- Review, Var, NA
*hepatoP↑, *Inflam↓, *antiOx↑, *lipid-P↓, *GSH↑, *SOD↑, *Catalase↑, *GPx↑, *GSTs↑, *ROS↓, *ALAT↓, *AST↓, *MDA↓, *NRF2↑, *COX2↑, *NF-kB↓, *ICAM-1↓, *MCP1↓, *HO-1↑, CXCc↓,
2821- CUR,    Antioxidant curcumin induces oxidative stress to kill tumor cells (Review)
- Review, Var, NA
*antiOx↑, *NRF2↑, *ROS↓, *Inflam↓, ROS↑, p‑ERK↑, ER Stress↑, mtDam↑, Apoptosis↑, Akt↓, mTOR↓, HO-1↑, Fenton↑, GSH↓, Iron↑, p‑JNK↑, Cyt‑c↑, ATF6↑, CHOP↑,
3574- CUR,    The effect of curcumin (turmeric) on Alzheimer's disease: An overview
- Review, AD, NA
*antiOx↑, *Inflam↓, *lipid-P↓, *cognitive↑, *memory↑, *Aβ↓, *COX2↓, *ROS↓, *AP-1↓, *NF-kB↓, *TNF-α↓, *IL1β↓, *SOD↑, *GSH↑, *HO-1↑, *IronCh↑, *BioAv↓, *Half-Life↝, *Dose↝, *BBB↑, *BioAv↑, *toxicity∅, *eff↑,
3576- CUR,    Protective Effects of Indian Spice Curcumin Against Amyloid-β in Alzheimer's Disease
- Review, AD, NA
*Inflam↓, *antiOx↑, *memory↑, *Aβ↓, *BBB↑, *cognitive↑, *tau↓, *LDL↓, *AChE↓, *IL1β↓, *IronCh↑, *neuroP↑, *BioAv↝, *PI3K↑, *Akt↑, *NRF2↑, *HO-1↑, *Ferritin↑, *HO-2↓, *ROS↓, *Ach↑, *GSH↑, *Bcl-2↑, *ChAT↑,
2688- CUR,    Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs
- Review, Var, NA - Review, AD, NA
*ROS↓, *SOD↑, p16↑, JAK2↓, STAT3↓, CXCL12↓, IL6↓, MMP2↓, MMP9↓, TGF-β↓, α-SMA↓, LAMs↓, DNAdam↑, *memory↑, *cognitive↑, *Inflam↓, *antiOx↑, *NO↑, *MDA↓, *ROS↓, DNMT1↓, ROS↑, Casp3↑, Apoptosis↑, miR-21↓, LC3II↓, ChemoSen↑, NF-kB↓, CSCs↓, Nanog↓, OCT4↓, SOX2↓, eff↑, Sp1/3/4↓, miR-27a-3p↓, ZBTB10↑, SOX9?, ChemoSen↑, VEGF↓, XIAP↓, Bcl-2↓, cycD1/CCND1↓, BioAv↑, Hif1a↓, EMT↓, BioAv↓, PTEN↑, VEGF↓, Akt↑, EZH2↓, NOTCH1↓, TP53↑, NQO1↑, HO-1↑,
3795- CUR,    Curcumin: A Golden Approach to Healthy Aging: A Systematic Review of the Evidence
- Review, AD, NA
*antiOx↑, *Inflam↓, *AntiAge↑, *AMPK↑, *SIRT1↑, *NF-kB↓, *mTOR↓, *NLRP3↓, *NADPH↓, *ROS↓, *COX2↓, *MCP1↓, *IL1β↓, *IL17↓, *IL23↓, *TNF-α↓, *MPO↓, *IL10↑, *lipid-P↓, *SOD↑, *Aβ↓, *p‑tau↓, *GSK‐3β↓, *CDK5↓, *TXNIP↓, *NRF2↑, *NQO1↑, *HO-1↑, *OS↑, *memory↑, *BDNF↑, *neuroP↑, *BACE↓, *AChE↓, *LDL↓,
3794- CUR,    Curcumin hybrid molecules for the treatment of Alzheimer's disease: Structure and pharmacological activities
- Review, AD, NA
*GSK‐3β↓, *CDK5↓, *p‑tau↓, *IronCh↑, *ROS↓, *HO-1↑, *SOD↑, *Catalase↑, *GSH↑, *TNF-α↓, *IL6↓, *IL12↓, *NRF2↑, *PPARγ↑, *IL4↑, *AChE↓, *Dose↝, *GutMicro↑,
1485- CUR,  Chemo,  Rad,    Curcumin, the golden spice from Indian saffron, is a chemosensitizer and radiosensitizer for tumors and chemoprotector and radioprotector for normal organs
- Review, Var, NA
ChemoSen↑, NF-kB↓, *STAT3↓, *COX2↓, *Akt↓, *NRF2↑, *HO-1↑, *GPx↑, *NADPH↑, *GSH↑, *ROS↓, *p300↓, radioP↑, chemoP↑, RadioS↑,
123- CUR,    Synthesis of novel 4-Boc-piperidone chalcones and evaluation of their cytotoxic activity against highly-metastatic cancer cells
- in-vitro, Colon, LoVo - in-vitro, Colon, COLO205 - in-vitro, Pca, PC3 - in-vitro, Pca, 22Rv1
NF-kB↓, ATF3↑, HO-1↑, Wnt↓, Akt↓, mTOR↓, PTEN↑, Apoptosis↑, TGF-β↓, PPARγ↑,
414- CUR,    Transcriptome Investigation and In Vitro Verification of Curcumin-Induced HO-1 as a Feature of Ferroptosis in Breast Cancer Cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
Ferroptosis↑, Iron↑, ROS↑, lipid-P↑, MDA↑, GSH↓, HO-1↑, NRF2↑, GPx↓, ROS↑, Iron↑, GPx4↓, HSP70/HSPA5↑, ATFs↑, CHOP↑, MDA↑, FTL↑, FTH1↑, BACH1↑, REL↑, USF1↑, NFE2L2↑,
2133- TQ,  CUR,  Cisplatin,    Thymoquinone and curcumin combination protects cisplatin-induced kidney injury, nephrotoxicity by attenuating NFκB, KIM-1 and ameliorating Nrf2/HO-1 signalling
- in-vitro, Nor, HEK293 - in-vivo, NA, NA
*creat↓, *TNF-α↓, *IL6↓, *MRP↓, *GFR↑, *mt-ATPase↑, *p‑Akt↑, *NRF2↑, *HO-1↑, *Casp3↓, *NF-kB↓, *RenoP↑,

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 ⓘ

ATF3↑, 1,   Fenton↑, 3,   Ferroptosis↑, 3,   GPx↓, 1,   GPx4↓, 3,   GSH↓, 4,   GSH/GSSG↓, 1,   H2O2↑, 1,   HO-1↑, 5,   Iron↑, 4,   lipid-P↑, 2,   MDA↑, 4,   NADH↓, 1,   NFE2L2↑, 1,   NQO1↑, 1,   NRF2↑, 3,   OXPHOS↓, 1,   ROS↑, 9,   ox-Trx1↑, 1,   TrxR↓, 1,   TrxR1↓, 1,  

Metal & Cofactor Biology ⓘ

FTH1↑, 1,   FTL↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   ETC↓, 1,   MMP↓, 2,   mtDam↑, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 2,   cMyc↓, 1,   FASN↓, 1,   G6PD↓, 1,   GLS↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   lactateProd↑, 1,   LDHA↓, 1,   PDK1↓, 1,   PKM2↓, 1,   PPARγ↑, 1,   SCD1↓, 1,   SREBP2↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 5,   Akt↑, 1,   Apoptosis↑, 6,   BAX↑, 1,   Bcl-2↓, 2,   Casp↑, 2,   Casp3↑, 1,   Cyt‑c↑, 2,   Ferroptosis↑, 3,   p‑JNK↑, 1,   MCT1↓, 1,  

Kinase & Signal Transduction ⓘ

SOX9?, 1,   Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

cJun↓, 1,   EZH2↓, 1,   HATs↓, 1,   miR-21↓, 1,   miR-27a-3p↓, 1,   USF1↑, 1,  

Protein Folding & ER Stress ⓘ

ATF6↑, 1,   ATFs↑, 1,   CHOP↑, 2,   ER Stress↑, 2,   HSP70/HSPA5↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↓, 1,   LC3II↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   DNMT1↓, 1,   DNMTs↓, 2,   p16↑, 1,   P53↑, 2,   TP53↑, 1,  

Cell Cycle & Senescence ⓘ

CDK4↓, 1,   cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 1,   CD133↑, 1,   cFos↓, 1,   CSCs↓, 2,   EMT↓, 2,   p‑ERK↑, 1,   FOXO1↓, 1,   GSK‐3β↓, 1,   HDAC↓, 2,   mTOR↓, 4,   Nanog↓, 1,   NOTCH1↓, 1,   OCT4↓, 1,   PI3K↓, 2,   PTEN↑, 2,   SOX2↓, 1,   STAT↓, 1,   STAT3↓, 2,   TumCG↓, 1,   Wnt↓, 3,  

Migration ⓘ

5LO↓, 1,   AP-1↓, 1,   BACH1↑, 1,   CXCL12↓, 1,   LAMs↓, 1,   MMP2↓, 1,   MMP9↓, 2,   MMPs↓, 2,   PKCδ↓, 1,   TGF-β↓, 2,   TumCI↓, 3,   TumCP↓, 1,   TumMeta↓, 3,   α-SMA↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   EGFR↓, 1,   Hif1a↓, 2,   REL↑, 1,   VEGF↓, 5,   ZBTB10↑, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 1,   COX2↓, 2,   CXCc↓, 1,   IL1↓, 1,   IL12↓, 1,   IL2↓, 1,   IL6↓, 2,   IL8↓, 1,   Imm↑, 1,   JAK↓, 1,   JAK2↓, 1,   MCP1↓, 1,   NF-kB↓, 6,   NK cell↑, 1,   PGE2↓, 1,  

Protein Aggregation ⓘ

XO↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   ChemoSen↑, 6,   eff↓, 1,   eff↑, 3,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   EZH2↓, 1,   GutMicro↑, 1,   IL6↓, 2,   TP53↑, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   chemoP↑, 1,   radioP↑, 1,  
Total Targets: 151

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 7,   Catalase↑, 3,   Ferroptosis↓, 1,   GPx↑, 2,   GSH↑, 5,   GSTs↑, 2,   HO-1↑, 12,   HO-2↓, 1,   Keap1↓, 1,   lipid-P↓, 3,   MDA↓, 3,   MPO↓, 1,   NQO1↑, 2,   NRF2↑, 11,   ROS↓, 12,   SOD↑, 6,  

Metal & Cofactor Biology ⓘ

Ferritin↑, 1,   IronCh↑, 4,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   AMPK↑, 2,   cytoP450↓, 1,   glucose↓, 1,   GlucoseCon↑, 1,   GLUT2↑, 1,   LDL↓, 2,   NADPH↓, 1,   NADPH↑, 1,   PPARγ↑, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 1,   Akt↑, 1,   p‑Akt↑, 1,   Bcl-2↑, 1,   Casp3↓, 1,   Ferroptosis↓, 1,   iNOS↓, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 2,   mTOR↓, 1,   p300↓, 1,   PI3K↑, 1,   STAT3↓, 1,  

Migration ⓘ

AP-1↓, 1,   mt-ATPase↑, 1,   CDK5↓, 2,   TXNIP↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↑, 1,  

Barriers & Transport ⓘ

BBB↑, 2,   GLUT3↑, 1,   GLUT4↑, 1,   MRP↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 4,   COX2↑, 1,   CRP↓, 1,   ICAM-1↓, 1,   IL1↓, 1,   IL10↑, 1,   IL12↓, 1,   IL17↓, 1,   IL1β↓, 3,   IL23↓, 1,   IL4↑, 1,   IL6↓, 4,   Inflam↓, 8,   MCP1↓, 2,   NF-kB↓, 4,   TNF-α↓, 6,  

Synaptic & Neurotransmission ⓘ

AChE↓, 4,   BDNF↑, 1,   ChAT↑, 1,   tau↓, 1,   p‑tau↓, 2,  

Protein Aggregation ⓘ

Aβ↓, 3,   BACE↓, 1,   NLRP3↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 3,   BioAv↑, 3,   BioAv↝, 1,   Dose↝, 2,   eff↑, 2,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   BMD↑, 1,   creat↓, 1,   CRP↓, 1,   Ferritin↑, 1,   GutMicro↑, 2,   IL6↓, 4,  

Functional Outcomes ⓘ

AntiAge↑, 1,   cognitive↑, 3,   GFR↑, 1,   hepatoP↑, 1,   memory↑, 4,   neuroP↑, 3,   OS↑, 1,   radioP↑, 1,   RenoP↑, 1,   toxicity∅, 1,  
Total Targets: 99

Scientific Paper Hit Count for: HO-1, HMOX1
16 Curcumin
2 Chemotherapy
1 Radiotherapy/Radiation
1 Thymoquinone
1 Cisplatin
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#:597  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

Home Page