HES1 Cancer Research Results

HES1, Hairy and Enhancer of Split 1: Click to Expand ⟱
Source:
Type:

HES1 - Hes Family BHLH Transcription Factor 1

Abbreviation: HES1

Alternative Names: Hairy and Enhancer of Split 1, Hairy/Enhancer-of-Split Homolog 1

Type: Basic helix-loop-helix transcription factor / transcriptional repressor / Notch pathway effector

Function: HES1 is a transcriptional regulator that controls cell differentiation, proliferation, stem/progenitor cell maintenance, cell-cycle progression, and apoptosis. It is a major downstream effector of canonical Notch signaling and can also be regulated by Hedgehog, Wnt, hypoxia, and other signaling pathways.

Cancer: ↑ HES1 is frequently overexpressed or aberrantly activated in cancer and can promote tumor-cell proliferation, stemness, epithelial-to-mesenchymal transition, invasion, metastasis, survival, immune evasion, and treatment resistance.

Favorable Direction in Cancer: ↓ HES1 expression or activity is generally favorable in cancers where HES1 functions as an oncogenic transcriptional regulator.

Pathway Relationship: NOTCH activation → NICD/RBPJ transcriptional complex → HES1 ↑ → differentiation suppression / stemness and survival programs ↑.

Interpretation Note: HES1 is strongly associated with Notch signaling but is not exclusively controlled by Notch. Changes in HES1 can therefore reflect crosstalk with Hedgehog, Wnt, hypoxia, JAK/STAT, PI3K/AKT/mTOR, and other pathways.
Scientific Papers found: Click to Expand⟱
8393- LT,    Progress, pharmacokinetics and future perspectives of luteolin modulating signaling pathways to exert anticancer effects: A review
- Review, Var, NA
TumCP↓, TumMeta↓, angioG↓, EMT↓, Imm↝, ChemoSen↑, *Inflam↓, *COX2/PTGS2↓, *NF-kB↓, MMP2↓, MMP9↓, p‑Akt↓, p‑PI3K↓, IGF-2↓, IGF-1R↓, CXCL16↓, NOTCH1↓, HES1↓, VEGF↓, ROS↑,
8401- LT,    Multi-Faceted Role of Luteolin in Cancer Metastasis: EMT, Angiogenesis, ECM Degradation and Apoptosis
- Review, Var, NA
EMT↓, N-cadherin↓, Vim↓, VEGF↓, VEGFR1↓, MMPs↓, Telomerase↓, NF-kB↓, cMyc↓, Bax:Bcl2↑, Casp3↑, PI3K↓, Akt↓, FOXO3↑, P21↑, p27/CDKN1B↑, cl‑PARP↑, Cyt‑c↑, NOTCH↓, HES1↓, ROS↑, SOD↓, miR-34b-5p↑, Hif1a↓, P21↓, survivin↓, Mcl-1?, Bcl-xL↓, MDM2↓, MMP2↓, MMP9↓, MMP3↓, MMP16↓, miR-384↑, NRF2↓, HO-1↓, angioG↓,
8348- Lut,    Lutein inhibits proliferation, invasion and migration of hypoxic breast cancer cells via downregulation of HES1
- in-vitro, BC, MCF7 - in-vitro, BC, MDA‑MB‑157
TumCP↓, Apoptosis↑, Hif1a↓, NOTCH↓, HES1↓, EMT↓, TumCI↓, TumCMig↓, ROS↓,

Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

CXCL16↓, 1,   HES1↓, 3,   MMP16↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

HO-1↓, 1,   NRF2↓, 1,   ROS↓, 1,   ROS↑, 2,   SOD↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

cMyc↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↑, 1,   Bax:Bcl2↑, 1,   Bcl-xL↓, 1,   Casp3↑, 1,   Cyt‑c↑, 1,   Mcl-1?, 1,   MDM2↓, 1,   p27/CDKN1B↑, 1,   survivin↓, 1,   Telomerase↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

cl‑PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

P21↓, 1,   P21↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

EMT↓, 3,   FOXO3↑, 1,   IGF-1R↓, 1,   IGF-2↓, 1,   NOTCH↓, 2,   NOTCH1↓, 1,   PI3K↓, 1,   p‑PI3K↓, 1,  

Migration(tgid=13) ⓘ

miR-384↑, 1,   MMP2↓, 2,   MMP3↓, 1,   MMP9↓, 2,   MMPs↓, 1,   N-cadherin↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 2,   TumMeta↓, 1,   VEGFR1↓, 1,   Vim↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 2,   Hif1a↓, 2,   miR-34b-5p↑, 1,   VEGF↓, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Imm↝, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,  
Total Targets: 51

Pathway results for Effect on Normal Cells:


Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   Inflam↓, 1,   NF-kB↓, 1,  
Total Targets: 3

Scientific Paper Hit Count for: HES1, Hairy and Enhancer of Split 1
2 Luteolin
1 Lutein
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:0  prod#:%  Target#:1814  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

Home Page