HO-1 Cancer Research Results

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.
Var, Various Cancer: Click to Expand ⟱
Cyclooxygenase (COX)-2 overexpression has been noted in various cancers. PI3Ks/AKT pathways are over-activated in several types of cancers.
EGFR altered activity has been noted in various pathological conditions. However, its regulation is an important step in the inhibition of cancer. In this regard, EGCG shows a pivotal role in the inhibition of EGFR activity.
Activating protein-1 transcription factor has been associated with pathogenesis including cancer.
Activation of the sonic hedgehog (Shh) pathway is required for the growth of numerous tissues and organs and recent evidence indicates that this pathway is often recruited to stimulate growth of cancer stem cells (CSCs) and to orchestrate the reprogramming of cancer cells via epithelial mesenchymal transition (EMT). Increased expression of Nanog has been associated with the aggressive nature of certain cancers, highlighting its role in promoting cancer stem cell characteristics.
The aberrant hedgehog (Hh)/GLI signaling pathway causes the formation and progression of a variety of tumors.
The process of cell apoptosis is often accompanied by the destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis.
Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses50.
Several studies have demonstrated that high cyclin D1 expression was observed in cancers including breast, lung, prostate, lymph node and colorectal cancers [23–25].
The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell.
Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure.
Heat shock proteins (HSPs) are normally induced under environmental stress to serve as chaperones for maintenance of correct protein folding but they are often overexpressed in many cancers, including breast cancer.
Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research.
Since increased Nrf2 gene expression is one of the main mechanisms of cancer cells in resisting chemotherapeutic drugs and survival in oxidative conditions; finding compounds with the ability to suppress Nrf2 gene expression with minimum side effects can be considered an important strategy for increasing the sensitivity of cancer cells to chemotherapy.
Overexpression of c-met stimulates proliferation, migration and invasion in various types of cancer including prostate cancer.
Overexpression of TGFα and EGFR by many carcinomas correlates with the development of cancer metastasis, resistance to chemotherapy and poor prognosis.
More than 50% of human cancers have a mutated nonfunctional p53.


Scientific Papers found: Click to Expand⟱
2296- Ba,    The most recent progress of baicalein in its anti-neoplastic effects and mechanisms
- Review, Var, NA
CDK1↓, Cyc↓, p27↑, P21↑, P53↑, TumCCA↑, TumCI↓, MMP2↓, MMP9↓, E-cadherin↑, N-cadherin↓, Vim↓, LC3A↑, p62↓, p‑mTOR↓, PD-L1↓, CAFs/TAFs↓, VEGF↓, ROCK1↓, Bcl-2↓, Bcl-xL↓, BAX↑, ROS↑, cl‑PARP↑, Casp3↑, Casp9↑, PTEN↑, MMP↓, Cyt‑c↑, Ca+2↑, PERK↑, IRE1↑, CHOP↑, Copper↑, Snail↓, Vim↓, Twist↓, GSH↓, NRF2↓, HO-1↓, GPx4↓, XIAP↓, survivin↓, DR5↑,
5536- BBM,    Regulation of Cell-Signaling Pathways by Berbamine in Different Cancers
- Review, Var, NA
JAK↝, STAT3↓, p‑CaMKII ↓, TGF-β↑, Smad1↑, ChemoSen↑, RadioS↑, TumCI↓, TumCMig↓, ROS↑, NRF2↓, SOD2↓, GPx1↓, HO-1↓,
5690- BJ,  BRU,    Brusatol: A potential sensitizing agent for cancer therapy from Brucea javanica
- Review, Var, NA
NRF2↓, TumCG↓, ChemoSen↑, ROS↑, NF-kB↓, Akt↓, mTOR↓, TumCCA↑, Apoptosis↑, PARP↑, Casp↑, P53↓, Bcl-2↓, PI3K↓, JAK2↓, EMT↓, p27↑, ROCK1↓, MMP2↓, MMP9↓, NRF2↓, AntiTum↑, HO-1↓, NQO1↓, VEGF↓, MRP1↓, RadioS↑, PhotoS↑, toxicity↝,
5680- BML,    Anticancer properties of bromelain: State-of-the-art and recent trends
- Review, Var, NA
*Inflam↓, *Bacteria↓, *Pain↓, *Diar↓, *Wound Healing↑, ERK↓, JNK↓, XIAP↓, HSP27↓, β-catenin/ZEB1↓, HO-1↓, lipid-P↓, ACSL4↑, ROS↑, SOD↑, Catalase↓, GSH↓, MDA↓, Casp3↓, Casp9↑, DNAdam↑, Apoptosis↑, NF-kB↓, P53↑, MAPK↓, APAF1↑, Cyt‑c↓, CD44↓, Imm↑, ATG5↑, LC3I↑, Beclin-1↑, IL2↓, IL4↓, IFN-γ↓, COX2↓, iNOS↓, ChemoSen↑, RadioS↑, Dose↝, other↓,
6017- CGA,    Therapeutic Potential of Chlorogenic Acid in Chemoresistance and Chemoprotection in Cancer Treatment
- Review, Var, NA
AntiCan↑, *chemoP↑, TNF-α↓, COX2↓, IL6↓, eff↑, PD-L1↓, *cognitive↓, *Aβ↓, *TAC↑, *SOD↑, *eff↑, *eff↑, ChemoSen↑, tumCV↓, Apoptosis↑, ERK↓, chemoP↑, *GPx↑, *GSTs↑, *GSH↑, *SOD↑, *Catalase↑, *ROS↓, *lipid-P↓, *MDA↓, *Casp3↓, *HO-1↓, cardioP↑, radioP↑,
2785- CHr,    Emerging cellular and molecular mechanisms underlying anticancer indications of chrysin
- Review, Var, NA
*NF-kB↓, *COX2↓, *iNOS↓, angioG↓, TOP1↓, HDAC↓, TNF-α↓, IL1β↓, cardioP↑, RenoP↑, neuroP↑, LDL↓, BioAv↑, eff↑, cycD1/CCND1↓, hTERT/TERT↓, MMP-10↓, Akt↓, STAT3↓, VEGF↓, EGFR↓, Snail↓, Slug↓, Vim↓, E-cadherin↑, eff↑, TET1↑, ROS↑, mTOR↓, PPARα↓, ER Stress↑, Ca+2↑, ERK↓, MMP↑, Cyt‑c↑, Casp3↑, HK2↓, NRF2↓, HO-1↓, MMP2↓, MMP9↓, Fibronectin↓, GRP78/BiP↑, XBP-1↓, p‑eIF2α↑, *AST↓, ALAT↓, ALP↓, LDH↓, COX2↑, Bcl-xL↓, IL6↓, PGE2↓, iNOS↓, DNAdam↑, UPR↑, Hif1a↓, EMT↓, Twist↓, lipid-P↑, CLDN1↓, PDK1↓, IL10↓, TLR4↓, NOTCH1↑, PARP↑, Mcl-1↓, XIAP↓,
1863- dietFMD,  Chemo,    Effect of fasting on cancer: A narrative review of scientific evidence
- Review, Var, NA
eff↑, ChemoSideEff↓, ChemoSen↑, Insulin↓, HDAC↓, IGF-1↓, STAT5↓, BG↓, MAPK↓, HO-1↓, ATG3↑, Beclin-1↑, p62↑, SIRT1↑, LAMP2↑, OXPHOS↑, ROS↑, P53↑, DNAdam↑, TumCD↑, ATP↑, Treg lymp↓, M2 MC↓, CD8+↑, Glycolysis↓, GutMicro↑, GutMicro↑, Warburg↓, Dose↝,
1846- dietFMD,  VitC,    A fasting-mimicking diet and vitamin C: turning anti-aging strategies against cancer
- Study, Var, NA
TumCG↓, ChemoSen↑, ChemoSideEff↓, ROS↑, Fenton↑, H2O2↑, eff↑, HO-1↓, DNAdam↑, eff↑,
1626- dietSTF,  dietFMD,    When less may be more: calorie restriction and response to cancer therapy
- Review, Var, NA
CRM↑, ChemoSen↑, RadioS↑, eff↑, eff↑, IGF-1↓, TumCG↓, AMPK↑, eff↑, ChemoSen↑, RadioS↑, ROS↑, DNAdam↑, eff↑, HO-1↓,
1605- EA,    Ellagic Acid and Cancer Hallmarks: Insights from Experimental Evidence
- Review, Var, NA
*BioAv↓, antiOx↓, Inflam↓, TumCP↓, TumCCA↑, cycD1/CCND1↓, cycE/CCNE↓, P53↑, P21↑, COX2↓, NF-kB↓, Akt↑, NOTCH↓, CDK2↓, CDK6↓, JAK↓, STAT3↓, EGFR↓, p‑ERK↓, p‑Akt↓, p‑STAT3↓, TGF-β↓, SMAD3↓, CDK6↓, Wnt/(β-catenin)↓, Myc↓, survivin↓, CDK8↓, PKCδ↓, tumCV↓, RadioS↑, eff↑, MDM2↓, XIAP↓, p‑RB1↓, PTEN↑, p‑FAK↓, Bax:Bcl2↑, Bcl-xL↓, Mcl-1↓, PUMA↑, NOXA↑, MMP↓, Cyt‑c↑, ROS↑, Ca+2↝, Endoglin↑, Diablo↑, AIF↑, iNOS↓, Casp9↑, Casp3↑, cl‑PARP↑, RadioS↑, Hif1a↓, HO-1↓, HO-2↓, SIRT1↓, selectivity↑, Dose∅, NHE1↓, Glycolysis↓, GlucoseCon↓, lactateProd↓, PDK1?, PDK1?, ECAR↝, COX1↓, Snail↓, Twist↓, cMyc↓, Telomerase↓, angioG↓, MMP2↓, MMP9↓, VEGF↓, Dose↝, PD-L1↓, eff↑, SIRT6↑, DNAdam↓,
1621- EA,    The multifaceted mechanisms of ellagic acid in the treatment of tumors: State-of-the-art
- Review, Var, NA
AntiCan↑, Apoptosis↑, TumCP↓, TumMeta↓, TumCI↓, TumAuto↑, VEGFR2↓, MAPK↓, PI3K↓, Akt↓, PD-1↓, NOTCH↓, PCNA↓, Ki-67↓, cycD1/CCND1↓, CDK2↑, CDK6↓, Bcl-2↓, cl‑PARP↑, BAX↑, Casp3↑, DR4↑, DR5↑, Snail↓, MMP2↓, MMP9↓, TGF-β↑, PKCδ↓, β-catenin/ZEB1↓, SIRT1↓, HO-1↓, ROS↑, CHOP↑, Cyt‑c↑, MMP↓, OCR↓, AMPK↑, Hif1a↓, NF-kB↓, E-cadherin↑, Vim↓, EMT↓, LC3II↑, CIP2A↓, GLUT1↓, PDH↝, MAD↓, LDH↓, GSTs↑, NOTCH↓, survivin↓, XIAP↓, ER Stress↑, ChemoSideEff↓, ChemoSen↑,
2894- HNK,    Pharmacological features, health benefits and clinical implications of honokiol
- Review, Var, NA - Review, AD, NA
*BioAv↓, *neuroP↑, *BBB↑, *ROS↓, *Keap1↑, *NRF2↑, *Casp3↓, *SIRT3↑, *Rho↓, *ERK↓, *NF-kB↓, angioG↓, RAS↓, PI3K↓, Akt↓, mTOR↓, *memory↑, *Aβ↓, *PPARγ↑, *PGC-1α↑, NF-kB↓, Hif1a↓, VEGF↓, HO-1↓, FOXM1↓, p27↑, P21↑, CDK2↓, CDK4↓, CDK6↓, cycD1/CCND1↓, Twist↓, MMP2↓, Rho↑, ROCK1↑, TumCMig↓, cFLIP↓, BMPs↑, OCR↑, ECAR↓, *AntiAg↑, *cardioP↑, *antiOx↑, *ROS↓, P-gp↓,
2914- LT,    Therapeutic Potential of Luteolin on Cancer
- Review, Var, NA
*antiOx↑, *IronCh↑, *toxicity↓, *BioAv↓, *BioAv↑, DNAdam↑, TumCP↓, DR5↑, P53↑, JNK↑, BAX↑, cl‑Casp3↑, cl‑Casp8↑, cl‑Casp9↑, cl‑PARP↑, survivin↓, cycD1/CCND1↓, CycB/CCNB1↓, CDC2↓, P21↑, angioG↓, MMP2↓, AEG1↓, VEGF↓, VEGFR2↓, MMP9↓, CXCR4↓, PI3K↓, Akt↓, ERK↓, TumAuto↑, LC3B-II↑, EMT↓, E-cadherin↑, N-cadherin↓, Wnt↓, ROS↑, NICD↓, p‑GSK‐3β↓, iNOS↓, COX2↓, NRF2↑, Ca+2↑, ChemoSen↑, ChemoSen↓, IFN-γ↓, RadioS↑, MDM2↓, NOTCH1↓, AR↓, TIMP1↑, TIMP2↑, ER Stress↑, CDK2↓, Telomerase↓, p‑NF-kB↑, p‑cMyc↑, hTERT/TERT↓, RAS↓, YAP/TEAD↓, TAZ↓, NF-kB↓, NRF2↓, HO-1↓, MDR1↓,
2919- LT,    Luteolin as a potential therapeutic candidate for lung cancer: Emerging preclinical evidence
- Review, Var, NA
RadioS↑, ChemoSen↑, chemoP↑, *lipid-P↓, *Catalase↑, *SOD↑, *GPx↑, *GSTs↑, *GSH↑, *TNF-α↓, *IL1β↓, *Casp3↓, *IL10↑, NRF2↓, HO-1↓, NQO1↓, GSH↓, MET↓, p‑MET↓, p‑Akt↓, HGF/c-Met↓, NF-kB↓, Bcl-2↓, SOD2↓, Casp8↑, Casp3↑, PARP↑, MAPK↓, NLRP3↓, ASC↓, Casp1↓, IL6↓, IKKα↓, p‑p65↓, p‑p38↑, MMP2↓, ICAM-1↓, EGFR↑, p‑PI3K↓, E-cadherin↓, ZO-1↑, N-cadherin↓, CLDN1↓, β-catenin/ZEB1↓, Snail↓, Vim↑, ITGB1↓, FAK↓, p‑Src↓, Rac1↓, Cdc42↓, Rho↓, PCNA↓, Tyro3↓, AXL↓, CEA↓, NSE↓, SOD↓, Catalase↓, GPx↓, GSR↓, GSTs↓, GSH↓, VitE↓, VitC↓, CYP1A1↓, cFos↑, AR↓, AIF↑, p‑STAT6↓, p‑MDM2↓, NOTCH1↓, VEGF↓, H3↓, H4↓, HDAC↓, SIRT1↓, ROS↑, DR5↑, Cyt‑c↑, p‑JNK↑, PTEN↓, mTOR↓, CD34↓, FasL↑, Fas↑, XIAP↓, p‑eIF2α↑, CHOP↑, LC3II↑, PD-1↓, STAT3↓, IL2↑, EMT↓, cachexia↓, BioAv↑, *Half-Life↝, *eff↑,

Showing Research Papers: 1 to 14 of 14

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 14

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   Catalase↓, 2,   Copper↑, 1,   CYP1A1↓, 1,   Fenton↑, 1,   GPx↓, 1,   GPx1↓, 1,   GPx4↓, 1,   GSH↓, 4,   GSR↓, 1,   GSTs↓, 1,   GSTs↑, 1,   H2O2↑, 1,   HO-1↓, 13,   HO-2↓, 1,   lipid-P↓, 1,   lipid-P↑, 1,   MAD↓, 1,   MDA↓, 1,   NQO1↓, 2,   NRF2↓, 7,   NRF2↑, 1,   OXPHOS↑, 1,   ROS↑, 12,   SOD↓, 1,   SOD↑, 1,   SOD2↓, 2,   VitC↓, 1,   VitE↓, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 2,   ATP↑, 1,   CDC2↓, 1,   Insulin↓, 1,   MMP↓, 3,   MMP↑, 1,   OCR↓, 1,   OCR↑, 1,   XIAP↓, 6,  

Core Metabolism/Glycolysis ⓘ

ACSL4↑, 1,   ALAT↓, 1,   AMPK↑, 2,   cMyc↓, 1,   p‑cMyc↑, 1,   CRM↑, 1,   ECAR↓, 1,   ECAR↝, 1,   GlucoseCon↓, 1,   Glycolysis↓, 2,   HK2↓, 1,   lactateProd↓, 1,   LDH↓, 2,   LDL↓, 1,   PDH↝, 1,   PDK1?, 2,   PDK1↓, 1,   PPARα↓, 1,   SIRT1↓, 3,   SIRT1↑, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 5,   Akt↑, 1,   p‑Akt↓, 2,   APAF1↑, 1,   Apoptosis↑, 4,   BAX↑, 3,   Bax:Bcl2↑, 1,   Bcl-2↓, 4,   Bcl-xL↓, 3,   Casp↑, 1,   Casp1↓, 1,   Casp3↓, 1,   Casp3↑, 5,   cl‑Casp3↑, 1,   Casp8↑, 1,   cl‑Casp8↑, 1,   Casp9↑, 3,   cl‑Casp9↑, 1,   cFLIP↓, 1,   Cyt‑c↓, 1,   Cyt‑c↑, 5,   Diablo↑, 1,   DR4↑, 1,   DR5↑, 4,   Fas↑, 1,   FasL↑, 1,   HGF/c-Met↓, 1,   hTERT/TERT↓, 2,   iNOS↓, 4,   JNK↓, 1,   JNK↑, 1,   p‑JNK↑, 1,   MAPK↓, 4,   Mcl-1↓, 2,   MDM2↓, 2,   p‑MDM2↓, 1,   Myc↓, 1,   NICD↓, 1,   NOXA↑, 1,   p27↑, 3,   p‑p38↑, 1,   PUMA↑, 1,   survivin↓, 4,   Telomerase↓, 2,   TumCD↑, 1,   YAP/TEAD↓, 1,  

Kinase & Signal Transduction ⓘ

p‑CaMKII ↓, 1,  

Transcription & Epigenetics ⓘ

H3↓, 1,   H4↓, 1,   other↓, 1,   PhotoS↑, 1,   tumCV↓, 2,  

Protein Folding & ER Stress ⓘ

CHOP↑, 3,   p‑eIF2α↑, 2,   ER Stress↑, 3,   GRP78/BiP↑, 1,   HSP27↓, 1,   IRE1↑, 1,   PERK↑, 1,   UPR↑, 1,   XBP-1↓, 1,  

Autophagy & Lysosomes ⓘ

ATG3↑, 1,   ATG5↑, 1,   Beclin-1↑, 2,   LAMP2↑, 1,   LC3A↑, 1,   LC3B-II↑, 1,   LC3I↑, 1,   LC3II↑, 2,   p62↓, 1,   p62↑, 1,   TumAuto↑, 2,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,   DNAdam↑, 6,   P53↓, 1,   P53↑, 5,   PARP↑, 3,   cl‑PARP↑, 4,   PCNA↓, 2,   SIRT6↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK2↓, 3,   CDK2↑, 1,   CDK4↓, 1,   Cyc↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 5,   cycE/CCNE↓, 1,   P21↑, 4,   p‑RB1↓, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

CD34↓, 1,   CD44↓, 1,   CDK8↓, 1,   cFos↑, 1,   CIP2A↓, 1,   EMT↓, 5,   ERK↓, 4,   p‑ERK↓, 1,   FOXM1↓, 1,   p‑GSK‐3β↓, 1,   HDAC↓, 3,   IGF-1↓, 2,   mTOR↓, 4,   p‑mTOR↓, 1,   NOTCH↓, 3,   NOTCH1↓, 2,   NOTCH1↑, 1,   PI3K↓, 4,   p‑PI3K↓, 1,   PTEN↓, 1,   PTEN↑, 2,   RAS↓, 2,   p‑Src↓, 1,   STAT3↓, 4,   p‑STAT3↓, 1,   STAT5↓, 1,   p‑STAT6↓, 1,   TAZ↓, 1,   TOP1↓, 1,   TumCG↓, 3,   Wnt↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

AEG1↓, 1,   AXL↓, 1,   Ca+2↑, 3,   Ca+2↝, 1,   CAFs/TAFs↓, 1,   Cdc42↓, 1,   CEA↓, 1,   CLDN1↓, 2,   E-cadherin↓, 1,   E-cadherin↑, 4,   FAK↓, 1,   p‑FAK↓, 1,   Fibronectin↓, 1,   ITGB1↓, 1,   Ki-67↓, 1,   MET↓, 1,   p‑MET↓, 1,   MMP-10↓, 1,   MMP2↓, 8,   MMP9↓, 6,   N-cadherin↓, 3,   PKCδ↓, 2,   Rac1↓, 1,   Rho↓, 1,   Rho↑, 1,   ROCK1↓, 2,   ROCK1↑, 1,   Slug↓, 1,   Smad1↑, 1,   SMAD3↓, 1,   Snail↓, 5,   TET1↑, 1,   TGF-β↓, 1,   TGF-β↑, 2,   TIMP1↑, 1,   TIMP2↑, 1,   Treg lymp↓, 1,   TumCI↓, 3,   TumCMig↓, 2,   TumCP↓, 3,   TumMeta↓, 1,   Twist↓, 4,   Tyro3↓, 1,   Vim↓, 4,   Vim↑, 1,   ZO-1↑, 1,   β-catenin/ZEB1↓, 3,  

Angiogenesis & Vasculature ⓘ

angioG↓, 4,   EGFR↓, 2,   EGFR↑, 1,   Endoglin↑, 1,   Hif1a↓, 4,   VEGF↓, 7,   VEGFR2↓, 2,  

Barriers & Transport ⓘ

GLUT1↓, 1,   NHE1↓, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

ASC↓, 1,   COX1↓, 1,   COX2↓, 4,   COX2↑, 1,   CXCR4↓, 1,   ICAM-1↓, 1,   IFN-γ↓, 2,   IKKα↓, 1,   IL10↓, 1,   IL1β↓, 1,   IL2↓, 1,   IL2↑, 1,   IL4↓, 1,   IL6↓, 3,   Imm↑, 1,   Inflam↓, 1,   JAK↓, 1,   JAK↝, 1,   JAK2↓, 1,   M2 MC↓, 1,   NF-kB↓, 7,   p‑NF-kB↑, 1,   p‑p65↓, 1,   PD-1↓, 2,   PD-L1↓, 3,   PGE2↓, 1,   TLR4↓, 1,   TNF-α↓, 2,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 2,   CDK6↓, 4,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 2,   ChemoSen↓, 1,   ChemoSen↑, 11,   Dose↝, 3,   Dose∅, 1,   eff↑, 12,   MDR1↓, 1,   MRP1↓, 1,   RadioS↑, 9,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   ALP↓, 1,   AR↓, 2,   BG↓, 1,   BMPs↑, 1,   CEA↓, 1,   EGFR↓, 2,   EGFR↑, 1,   FOXM1↓, 1,   GutMicro↑, 2,   hTERT/TERT↓, 2,   IL6↓, 3,   Ki-67↓, 1,   LDH↓, 2,   Myc↓, 1,   NSE↓, 1,   PD-L1↓, 3,  

Functional Outcomes ⓘ

AntiCan↑, 2,   AntiTum↑, 1,   cachexia↓, 1,   cardioP↑, 2,   chemoP↑, 2,   ChemoSideEff↓, 3,   neuroP↑, 1,   radioP↑, 1,   RenoP↑, 1,   toxicity↝, 1,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 308

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   Catalase↑, 2,   GPx↑, 2,   GSH↑, 2,   GSTs↑, 2,   HO-1↓, 1,   Keap1↑, 1,   lipid-P↓, 2,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 3,   SIRT3↑, 1,   SOD↑, 3,   TAC↑, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

PGC-1α↑, 1,  

Core Metabolism/Glycolysis ⓘ

PPARγ↑, 1,  

Cell Death ⓘ

Casp3↓, 3,   iNOS↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,  

Migration ⓘ

AntiAg↑, 1,   Rho↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL10↑, 1,   IL1β↓, 1,   Inflam↓, 1,   NF-kB↓, 2,   TNF-α↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 2,  

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

AST↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   chemoP↑, 1,   cognitive↓, 1,   memory↑, 1,   neuroP↑, 1,   Pain↓, 1,   toxicity↓, 1,   Wound Healing↑, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,   Diar↓, 1,  
Total Targets: 45

Scientific Paper Hit Count for: HO-1, HMOX1
3 diet FMD Fasting Mimicking Diet
2 Ellagic acid
2 Luteolin
1 Baicalein
1 Berbamine
1 Brucea javanica
1 brusatol
1 Bromelain
1 Chlorogenic acid
1 Chrysin
1 Chemotherapy
1 Vitamin C (Ascorbic Acid)
1 diet Short Term Fasting
1 Honokiol
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:26  Cells:%  prod#:%  Target#:597  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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