Acetyl-CoA Cancer Research Results
Acetyl-CoA, Acetyl-CoA/AcCoA: Click to Expand ⟱
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Acetyl-CoA:
A small molecule, specifically a coenzyme.
-Central to metabolism, especially in:
-The citric acid cycle (Krebs cycle)
-Fatty acid synthesis
-Ketogenesis
It carries acetyl groups (2-carbon units) and delivers them to biochemical reactions.
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Scientific Papers found: Click to Expand⟱
*CRM↓, AcCoA depleting agents (e.g., hydroxycitrate),
*Dose?, acetyltransferase inhibitors (e.g., anacardic acid, curcumin, epigallocatechin-3-gallate, garcinol, spermidine)
*AntiAge↑, Another common characteristic of these agents is their capacity to reduce aging-associated diseases and to confer protective responses against ischemia-induced organ damage.
*Acetyl-CoA↓, Altogether, these observations point to the idea that starvation causes autophagy because it results in the early depletion of AcCoA
*SIRT1↑, nduction of the deacetylase activity of sirtuins (as a result of changing NADH/NAD+ ratios and increased SIRT1 expression)
*AMPK↑, activation of AMPK activity (as a result of changing ATP/ADP ratios)
*mTORC1↓, inhibition of MTORC1 (as a result of amino acid depletion).
*AntiAge↑, CR or intermittent fasting are known for their wide life-span-extending
chemoP↑, fasting can reduce the subjective and objective toxicity of cytotoxic anticancer chemotherapies, both in humans and in mouse models, at the same time that it improves treatment outcome in mice
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in-vitro, |
Colon, |
HCT116 |
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Review, |
IBD, |
RAW264.7 |
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*Inflam↓, Modern research highlights Formononetin (FN) for its significant anti-inflammatory and extensively studied anti-cancer properties;
AntiCan↑,
*NF-kB↓, FN can inhibit the activation of the NF-κB/MAPK signaling pathways in LPS-induced RAW264.7 cells, thereby exerting its anti-inflammatory effects.
*MAPK↓,
*colonLen↑, FN significantly enhanced the colon length and DAI score in mice, notably suppressed the production of inflammatory cytokines, and inhibited the NF-κB/MAPK signaling pathway, leading to an improvement in DSS-induced colitis.
TumCG↓, FN significantly inhibited CT-26 and HCT116 cell growth, reduced tumor growth rate, improved pathological damage in CAC mice, and inhibited inflammatory factor production, enhancing intestinal mucosa protection.
Apoptosis↑, FN promoted apoptosis of colon cancer cells by increasing autophagy proteins (LC3, Beclin-1) and apoptosis proteins (CL-Caspase3, Bax), while reducing Bcl-2 expression.
LC3II↑,
Beclin-1↑,
cl‑Casp3↑,
BAX↑,
Bcl-2↓,
IGF-1↓, FN reduced IGF-1, ACLY, A-CoA, FAS, HSL, ATGL, and FFA levels, and increased GSK-3 levels
ACLY↓,
Acetyl-CoA↓,
Fas↓,
HSL/LIPE↓,
ATGL/PNPLA2↓,
FFA/NEFA↓,
GSK‐3β↑,
p‑mTOR↓, FN also inhibited the expression of P-mTOR, Rictor, P-Akt, ACLY, PDE3B, P-PKA, and P-HSL
Rictor↓,
p‑Akt↓,
PDE3B↓,
p‑PKA↓,
p‑HSL/LIPE↑,
TumAuto↑, FN significantly inhibits colon cancer cell growth and exerts anti-CAC effects by activating autophagy and apoptosis pathways and regulating lipid metabolism.
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in-vitro, |
AD, |
HEK293 |
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NA, |
Stroke, |
NA |
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in-vivo, |
AD, |
NA |
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*p‑tau↓, Resveratrol induces dephosphorylation of Tau
*PP2A↑, resveratrol, a polyphenol, significantly induces PP2A activity and reduces Tau phosphorylation at PP2A-dependent epitopes.
*neuroP↑, resveratrol is more and more being established as a neuroprotective drug after ischemic brain injury and in neurodegenerative disorders including Parkinson’s Disease13,14, AD15,16 and Huntington’s Disease
*antiOx↑, resveratrol has anti-oxidant activity19,20, inhibits cycloxygenase activity21,22, ribonucleotide reductase23, protein kinase C24, DNA polymerase 25 and has antiestrogenic properties26,27 and anti-platelet activity
COX2/PTGS2↓,
*AntiAg↑,
*SIRT1↑, it activates Sirt1, an NAD+-dependent protein deacetylase28,29 and also has been demonstrated to activate AMP kinase (AMPK)30,31, an important glucose sensor that inhibits acetyl-CoA carboxylase, thereby increasing oxidation of fatty acids and decre
*AMPK↑,
*Acetyl-CoA↓,
*FAO↑,
*ADAM10↑, Resveratrol has been suggested to induce the α-secretase ADAM10, which outcompetes BACE1 and thereby reduces Aβ-production
*BACE/β-secretase↓,
*Aβ↓,
*memory↑, interestingly, the resveratrol-mediated reduction of Aβ increases life span and improves learning and memory
*Inflam↓, reduces neuroinflammation47 and reduces oxidative stress48.
*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) ⓘ
ATGL/PNPLA2↓, 1, FFA/NEFA↓, 1, HSL/LIPE↓, 1, p‑HSL/LIPE↑, 1, PDE3B↓, 1, Rictor↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
Acetyl-CoA↓, 1, ACLY↓, 1,
Cell Death(tgid=5) ⓘ
p‑Akt↓, 1, Apoptosis↑, 1, BAX↑, 1, Bcl-2↓, 1, cl‑Casp3↑, 1, Fas↓, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
Beclin-1↑, 1, LC3II↑, 1, TumAuto↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
GSK‐3β↑, 1, IGF-1↓, 1, p‑mTOR↓, 1, TumCG↓, 1,
Migration(tgid=13) ⓘ
p‑PKA↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 1, chemoP↑, 1,
Total Targets: 25
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
colonLen↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 1, ROS↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
Acetyl-CoA↓, 2, AMPK↑, 2, CRM↓, 1, FAO↑, 1, SIRT1↑, 2,
Cell Death(tgid=5) ⓘ
MAPK↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
mTORC1↓, 1,
Migration(tgid=13) ⓘ
AntiAg↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
Inflam↓, 2, NF-kB↓, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
ADAM10↑, 1, p‑tau↓, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 1, BACE/β-secretase↓, 1, PP2A↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
Dose?, 1,
Functional Outcomes(tgid=23) ⓘ
AntiAge↑, 2, memory↑, 1, neuroP↑, 1,
Total Targets: 22
Scientific Paper Hit Count for: Acetyl-CoA, Acetyl-CoA/AcCoA
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#:% Target#:1348 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
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