HK2 Cancer Research Results

HK2, Hexokinase 2: Click to Expand ⟱
Source:
Type: enzyme
HK2 (Hexokinase 2) is an enzyme that plays a crucial role in glycolysis, the process by which cells convert glucose into energy. HK2 is a key regulatory enzyme in the glycolytic pathway, and it is primarily expressed in various tissues, including muscle, brain, and cancer cells.
HK2 has been shown to be overexpressed in many types of tumors, including breast, lung, and colon cancer. This overexpression may contribute to the development and progression of cancer by promoting glycolysis and energy production in cancer cells.
HK2 is a key regulatory enzyme in the glycolytic pathway.
HK2 plays a role in the regulation of glucose metabolism in diabetes.
HK2 is involved in the regulation of cell proliferation, apoptosis, and autophagy.

HK2 Inhibitors:
-2DG
-Curcumin
-Resveratrol
-EGCG
-Berberine
-Methyl Jasmonate (MJ)
-Honokiol
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⟱
2325- 2DG,    Research Progress of Warburg Effect in Hepatocellular Carcinoma
- Review, Var, NA
HK2↓, Glycolysis↓, PKM2↓, LDHA↓, TumCD↑, ChemoSen↑, eff↑,
2327- 2DG,    2-Deoxy-d-Glucose and Its Analogs: From Diagnostic to Therapeutic Agents
- Review, Var, NA
Glycolysis↓, HK2↓, mt-ROS↑, AMPK↑, PPP↓, NADPH↓, GSH↓, Bax:Bcl2↑, Apoptosis↑, RadioS↑, eff↓, Half-Life↓, other↝, eff↓,
5271- 3BP,    The anticancer agent 3-bromopyruvate: a simple but powerful molecule taken from the lab to the bedside
- Review, Var, NA
selectivity↑, selectivity↑, ATP↓, Glycolysis↓, HK2↓, mt-OXPHOS↓, GAPDH↓, mtDam↑, GSH↓, ROS↑, ER Stress↑, TumAuto↑, LC3‑Ⅱ/LC3‑Ⅰ↑, p62↓, Akt↓, HDAC↓, TumCA↑, Bcl-2↓, cMyc↓, Casp3↑, Cyt‑c↑, Mcl-1↓, PARP↓, ChemoSen↑,
5275- 3BP,    3-Bromopyruvate (3BP) a fast acting, promising, powerful, specific, and effective "small molecule" anti-cancer agent taken from labside to bedside: Introduction to a special issue
- Review, Var, NA
AntiCan↑, HK2↓, OCR↓,
5257- 3BP,    Tumor Energy Metabolism and Potential of 3-Bromopyruvate as an Inhibitor of Aerobic Glycolysis: Implications in Tumor Treatment
- Review, Var, NA
Glycolysis↓, mt-OXPHOS↓, HK2↓, Cyt‑c↑, Casp3↓, Bcl-2↓, Mcl-1↓, GAPDH↓, LDH↓, PDH↓, TCA↓, GlutaM↓, GSH↓, ATP↓, mitResp↓, ROS↑, ChemoSen↑, toxicity↝,
5266- 3BP,    3-bromopyruvate-based agent KAT-101
- Review, Var, NA
eff↑, Glycolysis↓, OXPHOS↓, ATP↓, TumCP↓, Apoptosis↑, HK2↓, MPT↑, LDH↓, PDH↓,
5267- 3BP,    Targeting Energy Metabolism in Cancer Treatment
- Review, Var, NA
HK2↓,
2324- ART/DHA,    Research Progress of Warburg Effect in Hepatocellular Carcinoma
- Review, Var, NA
PKM2↓, GLUT1↓, Glycolysis↓, Akt↓, mTOR↓, Hif1a↓, HK2↓, LDH↓, NF-kB↓,
2617- Ba,    Potential of baicalein in the prevention and treatment of cancer: A scientometric analyses based review
- Review, Var, NA
Ca+2↑, MMP2↓, MMP9↓, Vim↓, Snail↓, E-cadherin↑, Wnt↓, β-catenin/ZEB1↓, p‑Akt↓, p‑mTOR↓, NF-kB↓, i-ROS↑, Bcl-2↓, BAX↑, Cyt‑c↑, Casp3↑, Casp9↑, STAT3↓, IL6↓, MMP2↓, MMP9↓, NOTCH↓, PPARγ↓, p‑NRF2↓, HK2↓, LDHA↓, PDK1↓, Glycolysis↓, PTEN↑, Akt↓, Hif1a↓, MMP↓, VEGF↓, VEGFR2↓, TOP2↓, uPA↓, TIMP1↓, TIMP2↓, cMyc↓, TrxR↓, ASK1↑, Vim↓, ZO-1↑, E-cadherin↑, SOX2↓, OCT4↓, Shh↓, Smo↓, Gli1↓, N-cadherin↓, XIAP↓,
2616- Ba,    The Role of HK2 in Tumorigenesis and Development: Potential for Targeted Therapy with Natural Products
- Review, Var, NA
Glycolysis↓, HK2↓, LDHA↓, PDK1↓, PTEN↑,
2298- Ba,    Flavonoids Targeting HIF-1: Implications on Cancer Metabolism
- Review, Var, NA
TumCG↓, TumCP↓, Hif1a↓, VEGF↓, ChemoSen↑, Glycolysis↓, HK2↓, PDK1↓, LDHA↓, p‑Akt↓, PTEN↑,
2782- CHr,    Broad-Spectrum Preclinical Antitumor Activity of Chrysin: Current Trends and Future Perspectives
- Review, Var, NA - Review, Stroke, NA - Review, Park, NA
*antiOx↑, *Inflam↓, *hepatoP↑, *neuroP↑, *BioAv↓, *cardioP↑, *lipidLev↓, *RenoP↑, *TNF-α↓, *IL2↓, *PI3K↓, *Akt↓, *ROS↓, *cognitive↑, eff↑, cycD1/CCND1↓, hTERT/TERT↓, VEGF↓, p‑STAT3↓, TumMeta↓, TumCP↓, eff↑, eff↑, IL1β↓, IL6↓, NF-kB↓, ROS↑, MMP↓, Cyt‑c↑, Apoptosis↑, ER Stress↑, Ca+2↑, TET1↑, Let-7↑, Twist↓, EMT↓, TumCCA↑, Casp3↑, Casp9↑, BAX↑, HK2↓, GlucoseCon↓, lactateProd↓, Glycolysis↓, SHP1↑, N-cadherin↓, E-cadherin↑, UPR↑, PERK↑, ATF4↑, eIF2α↑, RadioS↑, NOTCH1↑, NRF2↓, BioAv↑, eff↑,
2784- CHr,    Chrysin targets aberrant molecular signatures and pathways in carcinogenesis (Review)
- Review, Var, NA
Apoptosis↑, TumCMig↓, *toxicity↝, ChemoSen↑, *BioAv↓, Dose↝, neuroP↑, *P450↓, *ROS↓, *HDL↑, *GSTs↑, *SOD↑, *Catalase↑, *MAPK↓, *NF-kB↓, *PTEN↑, *VEGF↑, ROS↑, MMP↓, Ca+2↑, selectivity↑, PCNA↓, Twist↓, EMT↓, CDKN1C↑, p‑STAT3↑, MMP2↓, MMP9↓, eff↑, cycD1/CCND1↓, hTERT/TERT↓, CLDN1↓, TumVol↓, OS↑, COX2↓, eff↑, CDK2↓, CDK4↓, selectivity↑, TumCCA↑, E-cadherin↑, HK2↓, HDAC↓,
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↓,
2790- CHr,    Chrysin: Pharmacological and therapeutic properties
- Review, Var, NA
*hepatoP↑, *neuroP↓, *ROS↓, *cardioP↑, *Inflam↓, eff↑, hTERT/TERT↓, cycD1/CCND1↓, MMP9↓, MMP2↓, TIMP1↑, TIMP2↑, BioAv↑, HK2↓, ROS↑, MMP↓, Casp3↑, ADP:ATP↑, Apoptosis↑, ER Stress↑, UPR↑, GRP78/BiP↝, eff↑, Ca+2↑,
1576- Citrate,    Targeting citrate as a novel therapeutic strategy in cancer treatment
- Review, Var, NA
TCA↓, T-Cell↝, Glycolysis↓, PKM2↓, PFK2?, SDH↓, PDH↓, β-oxidation↓, CPT1A↓, FASN↑, Casp3↑, Casp2↑, Casp8↑, Casp9↑, cl‑PARP↑, Hif1a↓, GLUT1↓, angioG↓, Ca+2↓, ROS↓, eff↓, Dose↓, eff↑, Mcl-1↓, HK2↓, IGF-1R↓, PTEN↑, citrate↓, Dose∅, eff↑, eff↑, eff↑, eff↑,
649- EGCG,  CUR,  PI,    Targeting Cancer Hallmarks with Epigallocatechin Gallate (EGCG): Mechanistic Basis and Therapeutic Targets
- Review, Var, NA
*BioEnh↑, EGFR↓, HER2/EBBR2↓, IGF-1↓, MAPK↓, ERK↓, RAS↓, Raf↓, NF-kB↓, p‑pRB↓, TumCCA↑, Glycolysis↓, Warburg↓, HK2↓, Pyruv↓,
2313- Flav,    Flavonoids against the Warburg phenotype—concepts of predictive, preventive and personalised medicine to cut the Gordian knot of cancer cell metabolism
- Review, Var, NA
Warburg↓, antiOx↑, angioG↓, Glycolysis↓, PKM2↓, PKM2:PKM1↓, β-catenin/ZEB1↓, cMyc↓, HK2↓, Akt↓, mTOR↓, GLUT1↓, Hif1a↓,
2438- Gra,    Emerging therapeutic potential of graviola and its constituents in cancers
- Review, Var, NA
Hif1a↓, GLUT1↓, GLUT4↓, HK2↓, LDHA↓, MUC4↓, TumCCA↑, MMP↓, NF-kB↓, ROS↓, Bax:Bcl2↑, ER(estro)↓, cycD1/CCND1↓, chemoPv↑, hepatoP↑,
2453- LE,    The Promoting Role of HK II in Tumor Development and the Research Progress of Its Inhibitors
- Review, Var, NA
HK2↓, PI3K↓, Akt↓, TumCP↓, Glycolysis↓,
2450- Matr,    The Promoting Role of HK II in Tumor Development and the Research Progress of Its Inhibitors
- Review, Var, NA
HK2↓, eff↓,
994- MET,    Tumor metabolism destruction via metformin-based glycolysis inhibition and glucose oxidase-mediated glucose deprivation for enhanced cancer therapy
- in-vitro, Var, NA
Glycolysis↓, HK2↓, ATP↓, AMPK↑, P53↑, Warburg↓, Apoptosis↑,
2451- PA,    The Promoting Role of HK II in Tumor Development and the Research Progress of Its Inhibitors
- Review, Var, NA
HK2↓, ATP↓, ROS↑,
1661- PBG,    Propolis: a natural compound with potential as an adjuvant in cancer therapy - a review of signaling pathways
- Review, Var, NA
JNK↓, ERK↓, Akt↓, NF-kB↓, FAK↓, MAPK↓, PI3K↓, Akt↓, P21↑, p27↑, TRAIL↑, BAX↑, P53↑, ERK↓, ChemoSen↑, RadioS↑, Glycolysis↓, HK2↓, PKM2↓, LDHA↓, PFK↓,
1664- PBG,    Anticancer Activity of Propolis and Its Compounds
- Review, Var, NA
Apoptosis↑, TumCMig↓, TumCCA↑, TumCP↓, angioG↓, P21↑, p27↑, CDK1↓, p‑CDK1↓, cycA1/CCNA1↓, CycB/CCNB1↓, P70S6K↓, CLDN2↓, HK2↓, PFK↓, PKM2↓, LDHA↓, TLR4↓, H3↓, α-tubulin↓, ROS↑, Akt↓, GSK‐3β↓, FOXO3↓, NF-kB↓, cycD1/CCND1↓, MMP↓, ROS↑, i-Ca+2↑, lipid-P↑, ER Stress↑, UPR↑, PERK↑, eIF2α↑, GRP78/BiP↑, BAX↑, PUMA↑, ROS↑, MMP↓, Cyt‑c↑, cl‑Casp8↑, cl‑Casp8↑, cl‑Casp3↑, cl‑PARP↑, eff↑, eff↑, RadioS↑, ChemoSen↑, eff↑,
1666- PBG,    Molecular and Cellular Mechanisms of Propolis and Its Polyphenolic Compounds against Cancer
- Review, Var, NA
ChemoSen↑, TumCCA↑, TumCP↓, Apoptosis↑, antiOx↓, ROS↑, COX2↑, ER(estro)↓, cycA1/CCNA1↓, CycB/CCNB1↓, CDK2↓, P21↑, p27↑, hTERT/TERT↓, HDAC↓, ROS⇅, Dose?, ROS↓, ROS↑, DNAdam↑, ChemoSen↑, LOX1↓, lipid-P↓, NO↑, Igs↑, NK cell↑, MMPs↓, VEGF↓, Hif1a↓, GLUT1↓, HK2↓, selectivity↑, RadioS↑, GlucoseCon↓, lactateProd↓, eff↓, *BioAv↓,
2380- PBG,    Potential Strategies for Overcoming Drug Resistance Pathways Using Propolis and Its Polyphenolic/Flavonoid Compounds in Combination with Chemotherapy and Radiotherapy
- Review, Var, NA
Hif1a↓, Glycolysis↓, PKM2↓, LDHA↓, GLUT2↓, HK2↓, PFK1↓, PDK1↓, chemoP↓, radioP↑,
2946- PL,    Piperlongumine, a potent anticancer phytotherapeutic: Perspectives on contemporary status and future possibilities as an anticancer agent
- Review, Var, NA
ROS↑, GSH↓, DNAdam↑, ChemoSen↑, RadioS↑, BioEnh↑, selectivity↑, BioAv↓, eff↑, p‑Akt↓, mTOR↓, GSK‐3β↓, β-catenin/ZEB1↓, HK2↓, Glycolysis↓, Cyt‑c↑, Casp9↑, Casp3↑, Casp7↑, cl‑PARP↑, TrxR↓, ER Stress↑, ATF4↝, CHOP↑, Prx4↑, NF-kB↓, cycD1/CCND1↓, CDK4↓, CDK6↓, p‑RB1↓, RAS↓, cMyc↓, TumCCA↑, selectivity↑, STAT3↓, NRF2↑, HO-1↑, PTEN↑, P-gp↓, MDR1↓, MRP1↓, survivin↓, Twist↓, AP-1↓, Sp1/3/4↓, STAT1↓, STAT6↓, SOX4↑, XBP-1↑, P21↑, eff↑, Inflam↓, COX2↓, IL6↓, MMP9↓, TumMeta↓, TumCI↓, ICAM-1↓, CXCR4↓, VEGF↓, angioG↓, Half-Life↝, BioAv↑,
2948- PL,    The promising potential of piperlongumine as an emerging therapeutics for cancer
- Review, Var, NA
tumCV↓, TumCP↓, TumCI↓, angioG↓, EMT↓, TumMeta↓, *hepatoP↑, *lipid-P↓, *GSH↑, cardioP↑, CycB/CCNB1↓, cycD1/CCND1↓, CDK2↓, CDK1↓, CDK4↓, CDK6↓, PCNA↓, Akt↓, mTOR↓, Glycolysis↓, NF-kB↓, IKKα↓, JAK1↓, JAK2↓, STAT3↓, ERK↓, cFos↓, Slug↓, E-cadherin↑, TOP2↓, P53↑, P21↑, Bcl-2↓, BAX↑, Casp3↑, Casp7↑, Casp8↑, p‑HER2/EBBR2↓, HO-1↑, NRF2↑, BIM↑, p‑FOXO3↓, Sp1/3/4↓, cMyc↓, EGFR↓, survivin↓, cMET↓, NQO1↑, SOD2↑, TrxR↓, MDM2↓, p‑eIF2α↑, ATF4↑, CHOP↑, MDA↑, Ki-67↓, MMP9↓, Twist↓, SOX2↓, Nanog↓, OCT4↓, N-cadherin↓, Vim↓, Snail↓, TumW↓, TumCG↓, HK2↓, RB1↓, IL6↓, IL8↓, SOD1↑, RadioS↑, ChemoSen↑, toxicity↓, Sp1/3/4↓, GSH↓, SOD↑,
2300- QC,    Flavonoids Targeting HIF-1: Implications on Cancer Metabolism
- Review, Var, NA
AntiTum↑, Hif1a↓, *Hif1a↑, Glycolysis↓, HK2↓, PDK3↓, PFKP?,
2334- RES,    Glut 1 in Cancer Cells and the Inhibitory Action of Resveratrol as A Potential Therapeutic Strategy
- Review, Var, NA
GLUT1↓, GlucoseCon↓, lactateProd↓, Akt↓, mTOR↓, Dose↝, SIRT6↑, PKM2↓, HK2↓, PFK1↓, ChemoSen↑,
2332- RES,    Resveratrol’s Anti-Cancer Effects through the Modulation of Tumor Glucose Metabolism
- Review, Var, NA
Glycolysis↓, GLUT1↓, PFK1↓, Hif1a↓, ROS↑, PDH↑, AMPK↑, TumCG↓, TumCI↓, TumCP↓, p‑NF-kB↓, SIRT1↑, SIRT3↑, LDH↓, PI3K↓, mTOR↓, PKM2↓, R5P↝, G6PD↓, TKT↝, talin↓, HK2↓, GRP78/BiP↑, GlucoseCon↓, ER Stress↑, Warburg↓, PFK↓,
2441- RES,    Anti-Cancer Properties of Resveratrol: A Focus on Its Impact on Mitochondrial Functions
- Review, Var, NA
*toxicity↓, *BioAv↝, *Dose↝, *hepatoP↑, *neuroP↑, *AntiAg↑, *COX2↓, *antiOx↑, *ROS↓, *ROS↑, PI3K↓, Akt↓, NF-kB↓, Wnt↓, β-catenin/ZEB1↓, NRF2↑, GPx↑, HO-1↑, BioEnh?, PTEN↑, ChemoSen↑, eff↑, mt-ROS↑, Warburg↓, Glycolysis↓, GlucoseCon↓, GLUT1↓, lactateProd↓, HK2↓, EGFR↓, cMyc↓, ROS↝, MMPs↓, MMP7↓, survivin↓, TumCP↓, TumCMig↓, TumCI↓,
2411- UA,    Ursolic acid in health and disease
- Review, Var, NA
Inflam↓, antiOx↑, NF-kB↓, Bcl-xL↓, Bcl-2↓, cycD1/CCND1↓, Ki-67↓, CD31↓, STAT3↓, EGFR↓, P53↑, P21↓, HK2↓, PKM2↓, ATP↓, lactateProd↓, p‑ERK↓, MMP↓, NO↑, ATM↑, Casp3↑, AMPK↑, JNK↑, FAO↑, FASN↓, *GSH↑, *SOD↑, *Catalase↑, *GPx↑, *GSTs↑, neuroP↑,
5021- UA,    Anticancer effect of ursolic acid via mitochondria-dependent pathways
- Review, Var, NA
Inflam↓, TNF-α↓, IL6↓, IL17↓, NF-kB↓, COX2↓, *AntiDiabetic↑, *hepatoP↑, ALAT↓, AST↓, TumCP↓, Apoptosis↑, TumCCA↑, TumAuto↑, tumCV↓, TumCMig↓, Glycolysis↓, ATP↓, lactateProd↓, HK2↓, PKA↓, COX2↓, mtDam↑, Casp3↑, Casp8↑, Casp9↑, Akt↓, ROS↑, MMP↓, P53↑,
2301- Wog,    Flavonoids Targeting HIF-1: Implications on Cancer Metabolism
- Review, Var, NA
HK2↓, PDK1↓, LDHA↓, Hif1a↓, PI3K↓, Akt↓, Glycolysis↓, P53↑, GLUT1↓,
2397- Wor,    Phytochemicals targeting glycolysis in colorectal cancer therapy: effects and mechanisms of action
- Review, Var, NA
lactateProd↓, GlucoseCon↓, GLUT3↓, HK2↓, PKM2↓, LDHA↓,

Showing Research Papers: 1 to 37 of 37

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 37

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   antiOx↑, 2,   GPx↑, 1,   GSH↓, 5,   HO-1↓, 1,   HO-1↑, 3,   lipid-P↓, 1,   lipid-P↑, 2,   MDA↑, 1,   NQO1↑, 1,   NRF2↓, 2,   NRF2↑, 3,   p‑NRF2↓, 1,   OXPHOS↓, 1,   mt-OXPHOS↓, 2,   Prx4↑, 1,   ROS↓, 3,   ROS↑, 15,   ROS⇅, 1,   ROS↝, 1,   i-ROS↑, 1,   mt-ROS↑, 2,   SIRT3↑, 1,   SOD↑, 1,   SOD1↑, 1,   SOD2↑, 1,   TKT↝, 1,   TrxR↓, 3,  

Mitochondria & Bioenergetics ⓘ

ADP:ATP↑, 1,   ATP↓, 7,   mitResp↓, 1,   MMP↓, 9,   MMP↑, 1,   MPT↑, 1,   mtDam↑, 2,   OCR↓, 1,   Raf↓, 1,   SDH↓, 1,   XIAP↓, 2,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 2,   AMPK↑, 4,   citrate↓, 1,   cMyc↓, 6,   CPT1A↓, 1,   FAO↑, 1,   FASN↓, 1,   FASN↑, 1,   G6PD↓, 1,   GAPDH↓, 2,   GlucoseCon↓, 6,   GLUT2↓, 1,   GlutaM↓, 1,   Glycolysis↓, 24,   HK2↓, 37,   lactateProd↓, 7,   LDH↓, 5,   LDHA↓, 10,   LDL↓, 1,   NADPH↓, 1,   PDH↓, 3,   PDH↑, 1,   PDK1↓, 6,   PDK3↓, 1,   PFK↓, 3,   PFK1↓, 3,   PFK2?, 1,   PFKP?, 1,   PKM2↓, 11,   PKM2:PKM1↓, 1,   PPARα↓, 1,   PPARγ↓, 1,   PPP↓, 1,   Pyruv↓, 1,   R5P↝, 1,   SIRT1↑, 1,   TCA↓, 2,   Warburg↓, 5,   β-oxidation↓, 1,  

Cell Death ⓘ

Akt↓, 14,   p‑Akt↓, 3,   Apoptosis↑, 9,   ASK1↑, 1,   BAX↑, 5,   Bax:Bcl2↑, 2,   Bcl-2↓, 5,   Bcl-xL↓, 2,   BIM↑, 1,   Casp2↑, 1,   Casp3↓, 1,   Casp3↑, 10,   cl‑Casp3↑, 1,   Casp7↑, 2,   Casp8↑, 3,   cl‑Casp8↑, 2,   Casp9↑, 5,   Cyt‑c↑, 7,   hTERT/TERT↓, 5,   iNOS↓, 1,   JNK↓, 1,   JNK↑, 1,   MAPK↓, 2,   Mcl-1↓, 4,   MDM2↓, 1,   p27↑, 3,   PUMA↑, 1,   survivin↓, 3,   TRAIL↑, 1,   TumCD↑, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,   p‑HER2/EBBR2↓, 1,   Sp1/3/4↓, 3,  

Transcription & Epigenetics ⓘ

H3↓, 1,   other↝, 1,   p‑pRB↓, 1,   tumCV↓, 2,  

Protein Folding & ER Stress ⓘ

CHOP↑, 2,   eIF2α↑, 2,   p‑eIF2α↑, 2,   ER Stress↑, 7,   GRP78/BiP↑, 3,   GRP78/BiP↝, 1,   PERK↑, 2,   UPR↑, 4,   XBP-1↓, 1,   XBP-1↑, 1,  

Autophagy & Lysosomes ⓘ

LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   p62↓, 1,   TumAuto↑, 2,  

DNA Damage & Repair ⓘ

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

Cell Cycle & Senescence ⓘ

CDK1↓, 2,   p‑CDK1↓, 1,   CDK2↓, 3,   CDK4↓, 3,   cycA1/CCNA1↓, 2,   CycB/CCNB1↓, 3,   cycD1/CCND1↓, 9,   P21↓, 1,   P21↑, 5,   RB1↓, 1,   p‑RB1↓, 1,   TumCCA↑, 8,  

Proliferation, Differentiation & Cell State ⓘ

cFos↓, 1,   cMET↓, 1,   EMT↓, 4,   ERK↓, 5,   p‑ERK↓, 1,   FOXO3↓, 1,   p‑FOXO3↓, 1,   Gli1↓, 1,   GSK‐3β↓, 2,   HDAC↓, 4,   IGF-1↓, 1,   IGF-1R↓, 1,   Let-7↑, 1,   mTOR↓, 7,   p‑mTOR↓, 1,   Nanog↓, 1,   NOTCH↓, 1,   NOTCH1↑, 2,   OCT4↓, 2,   P70S6K↓, 1,   PI3K↓, 5,   PTEN↑, 6,   RAS↓, 2,   Shh↓, 1,   SHP1↑, 1,   Smo↓, 1,   SOX2↓, 2,   STAT1↓, 1,   STAT3↓, 5,   p‑STAT3↓, 1,   p‑STAT3↑, 1,   STAT6↓, 1,   TOP1↓, 1,   TOP2↓, 2,   TumCG↓, 3,   Wnt↓, 2,  

Migration ⓘ

AP-1↓, 1,   Ca+2↓, 1,   Ca+2↑, 5,   i-Ca+2↑, 1,   CD31↓, 1,   CDKN1C↑, 1,   CLDN1↓, 2,   CLDN2↓, 1,   E-cadherin↑, 6,   FAK↓, 1,   Fibronectin↓, 1,   Ki-67↓, 2,   MMP-10↓, 1,   MMP2↓, 5,   MMP7↓, 1,   MMP9↓, 7,   MMPs↓, 2,   MUC4↓, 1,   N-cadherin↓, 3,   PKA↓, 1,   Slug↓, 2,   Snail↓, 3,   SOX4↑, 1,   talin↓, 1,   TET1↑, 2,   TIMP1↓, 1,   TIMP1↑, 1,   TIMP2↓, 1,   TIMP2↑, 1,   TumCA↑, 1,   TumCI↓, 4,   TumCMig↓, 4,   TumCP↓, 10,   TumMeta↓, 3,   Twist↓, 5,   uPA↓, 1,   Vim↓, 4,   ZO-1↑, 1,   α-tubulin↓, 1,   β-catenin/ZEB1↓, 4,  

Angiogenesis & Vasculature ⓘ

angioG↓, 6,   ATF4↑, 2,   ATF4↝, 1,   EGFR↓, 5,   Hif1a↓, 12,   LOX1↓, 1,   NO↑, 2,   VEGF↓, 6,   VEGFR2↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 9,   GLUT3↓, 1,   GLUT4↓, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 4,   COX2↑, 2,   CXCR4↓, 1,   ICAM-1↓, 1,   Igs↑, 1,   IKKα↓, 1,   IL10↓, 1,   IL17↓, 1,   IL1β↓, 2,   IL6↓, 6,   IL8↓, 1,   Inflam↓, 3,   JAK1↓, 1,   JAK2↓, 1,   NF-kB↓, 12,   p‑NF-kB↓, 1,   NK cell↑, 1,   PGE2↓, 1,   T-Cell↝, 1,   TLR4↓, 2,   TNF-α↓, 2,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 2,   ER(estro)↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 4,   BioEnh?, 1,   BioEnh↑, 1,   ChemoSen↑, 13,   Dose?, 1,   Dose↓, 1,   Dose↝, 2,   Dose∅, 1,   eff↓, 5,   eff↑, 23,   Half-Life↓, 1,   Half-Life↝, 1,   MDR1↓, 1,   MRP1↓, 1,   RadioS↑, 7,   selectivity↑, 7,  

Clinical Biomarkers ⓘ

ALAT↓, 2,   ALP↓, 1,   AST↓, 1,   EGFR↓, 5,   HER2/EBBR2↓, 1,   p‑HER2/EBBR2↓, 1,   hTERT/TERT↓, 5,   IL6↓, 6,   Ki-67↓, 2,   LDH↓, 5,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 1,   cardioP↑, 2,   chemoP↓, 1,   chemoPv↑, 1,   hepatoP↑, 1,   neuroP↑, 3,   OS↑, 1,   radioP↑, 1,   RenoP↑, 1,   toxicity↓, 1,   toxicity↝, 1,   TumVol↓, 1,   TumW↓, 1,  
Total Targets: 301

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   Catalase↑, 2,   GPx↑, 1,   GSH↑, 2,   GSTs↑, 2,   HDL↑, 1,   lipid-P↓, 1,   ROS↓, 4,   ROS↑, 1,   SOD↑, 2,  

Core Metabolism/Glycolysis ⓘ

lipidLev↓, 1,  

Cell Death ⓘ

Akt↓, 1,   iNOS↓, 1,   MAPK↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 1,   PTEN↑, 1,  

Migration ⓘ

AntiAg↑, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↑, 1,   VEGF↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   IL2↓, 1,   Inflam↓, 2,   NF-kB↓, 2,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 3,   BioAv↝, 1,   BioEnh↑, 1,   Dose↝, 1,   P450↓, 1,  

Clinical Biomarkers ⓘ

AST↓, 1,  

Functional Outcomes ⓘ

AntiDiabetic↑, 1,   cardioP↑, 2,   cognitive↑, 1,   hepatoP↑, 5,   neuroP↓, 1,   neuroP↑, 2,   RenoP↑, 1,   toxicity↓, 1,   toxicity↝, 1,  
Total Targets: 39

Scientific Paper Hit Count for: HK2, Hexokinase 2
5 3-bromopyruvate
4 Chrysin
4 Propolis -bee glue
3 Baicalein
3 Resveratrol
2 2-DeoxyGlucose
2 Piperlongumine
2 Ursolic acid
1 Artemisinin
1 Citric Acid
1 EGCG (Epigallocatechin Gallate)
1 Curcumin
1 Piperine
1 flavonoids
1 Graviola
1 Licorice
1 Matrine
1 Metformin
1 Pachymic acid
1 Quercetin
1 Wogonin
1 Worenine
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#:773  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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