ACC Cancer Research Results

ACC, Acetyl-CoA Carboxylase: Click to Expand ⟱
Source:
Type: enzyme
ACC-α (Acetyl-CoA Carboxylase alpha) is a cytosolic isoform of ACC that is primarily involved in the regulation of fatty acid synthesis in lipogenic tissues, such as liver and adipose tissue. ACC-α is a key enzyme in the biosynthesis of fatty acids, particularly in the context of de novo lipogenesis.
ACC is a biotin-containing enzyme that exists in two main isoforms: ACC-α and ACC-β.
Overexpression of ACC-α has been linked to increased fatty acid synthesis, which can contribute to cancer cell growth and survival.
ACC-β (Acetyl-CoA Carboxylase beta) is a mitochondrial isoform of ACC that is primarily involved in the regulation of fatty acid oxidation.
In general, high ACC expression is associated with:
- Poor prognosis
- Increased tumor size
- Metastasis
- Resistance to chemotherapy
-Poor response to treatment
Low ACC expression is associated with:
- Better prognosis
- Smaller tumor size
- Less metastasis
- Better response to chemotherapy
- Better response to treatment
Scientific Papers found: Click to Expand⟱
1186- GAs,    Ginkgolic acid suppresses the development of pancreatic cancer by inhibiting pathways driving lipogenesis
- in-vitro, PC, NA - in-vitro, Nor, HUVECs - in-vivo, PC, NA
tumCV↓, *toxicity∅, TumCMig↓, TumCI↓, Apoptosis↑, AMPK↑, lipoGen↓, ACC↓, FASN↓,
7793- ISQ,    Apoptosis triggered by isoquercitrin in bladder cancer cells by activating the AMPK-activated protein kinase pathway
- in-vitro, Bladder, T24/HTB-9
tumCV↓, ROS↑, AMPK↑, Glycolysis↓, p‑PI3K↓, p‑Akt↓, Casp↑, mTOR↓, ACC↓, FASN↓,
2545- M-Blu,    Reversing the Warburg Effect as a Treatment for Glioblastoma
- in-vitro, GBM, U87MG - NA, AD, NA - in-vitro, GBM, A172 - in-vitro, GBM, T98G
Warburg↓, OCR↑, lactateProd↓, TumCP↓, TumCCA↑, AMPK↑, ACC↓, Cyc↓, neuroP↑, Cyt‑c↝, Glycolysis↓, ECAR↓, TumCG↓, other↓,
1231- PBG,    Caffeic acid phenethyl ester inhibits MDA-MB-231 cell proliferation in inflammatory microenvironment by suppressing glycolysis and lipid metabolism
- in-vitro, BC, MDA-MB-231
TumCP↓, TumCMig↓, TumCI↓, MMP↓, TLR4↓, TNF-α↓, NF-kB↓, IL1β↓, IL6↓, IRAK4↓, GLUT1↓, GLUT3↓, HK2↓, PFK↓, PKM2↓, LDHA↓, ACC↓, FASN↓, eff↓,
3381- QC,    Quercetin induces cell death in cervical cancer by reducing O-GlcNAcylation of adenosine monophosphate-activated protein kinase
- in-vitro, Cerv, HeLa
SREBP1/SREBF1↓, TumCP↓, TumCD↑, AMPK↑, SREBP1/SREBF1↓, FASN↓, ACC↓,
3200- SFN,    Sulforaphane suppresses the activity of sterol regulatory element-binding proteins (SREBPs) by promoting SREBP precursor degradation
- in-vitro, Liver, HUH7
FASN↓, ACC↓, SREBP1/SREBF1↓,
964- SIL,    Silibinin inhibits hypoxia-induced HIF-1α-mediated signaling, angiogenesis and lipogenesis in prostate cancer cells: In vitro evidence and in vivo functional imaging and metabolomics
- vitro+vivo, Pca, LNCaP - in-vitro, Pca, 22Rv1
TumCP↓, Hif1a↓, NADPH↓, angioG↓, FASN↓, ACC↓,
1214- VitK2,    Vitamin K2 promotes PI3K/AKT/HIF-1α-mediated glycolysis that leads to AMPK-dependent autophagic cell death in bladder cancer cells
- in-vitro, Bladder, T24/HTB-9 - in-vitro, Bladder, J82
Glycolysis↑, GlucoseCon↑, lactateProd↑, TCA↓, PI3K↑, Akt↑, AMPK↑, mTORC1↓, TumAuto↑, GLUT1↑, HK2↑, LDHA↑, ACC↓, PDH↓, eff↓, cMyc↓, Hif1a↑, p‑Akt↑, eff↓, eff↓, eff↓, eff↓, ROS↑,

Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 1,   OCR↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACC↓, 8,   AMPK↑, 5,   cMyc↓, 1,   ECAR↓, 1,   FASN↓, 6,   GlucoseCon↑, 1,   Glycolysis↓, 2,   Glycolysis↑, 1,   HK2↓, 1,   HK2↑, 1,   lactateProd↓, 1,   lactateProd↑, 1,   LDHA↓, 1,   LDHA↑, 1,   lipoGen↓, 1,   NADPH↓, 1,   PDH↓, 1,   PFK↓, 1,   PKM2↓, 1,   SREBP1/SREBF1↓, 3,   TCA↓, 1,   Warburg↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↑, 1,   p‑Akt↓, 1,   p‑Akt↑, 1,   Apoptosis↑, 1,   Casp↑, 1,   Cyt‑c↝, 1,   TumCD↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↓, 1,   tumCV↓, 2,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

Cyc↓, 1,   TumCCA↑, 1,  

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

mTOR↓, 1,   mTORC1↓, 1,   PI3K↑, 1,   p‑PI3K↓, 1,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

TumCI↓, 2,   TumCMig↓, 2,   TumCP↓, 4,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   Hif1a↓, 1,   Hif1a↑, 1,  

Barriers & Transport(tgid=15) ⓘ

GLUT1↓, 1,   GLUT1↑, 1,   GLUT3↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL1β↓, 1,   IL6↓, 1,   IRAK4↓, 1,   NF-kB↓, 1,   TLR4↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↓, 6,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

neuroP↑, 1,  
Total Targets: 60

Pathway results for Effect on Normal Cells:


Functional Outcomes(tgid=23) ⓘ

toxicity∅, 1,  
Total Targets: 1

Scientific Paper Hit Count for: ACC, Acetyl-CoA Carboxylase
1 Ginkgolic acids
1 isoquercitrin
1 Methylene blue
1 Propolis -bee glue
1 Quercetin
1 Sulforaphane (mainly Broccoli)
1 Silymarin (Milk Thistle) silibinin
1 Vitamin K2
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#:932  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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