ACC Cancer Research Results
ACC, Acetyl-CoA Carboxylase: Click to Expand ⟱
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| 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
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Scientific Papers found: Click to Expand⟱
*ECAR↑, Baicalin promoted metabolic reprogramming in 3T3-L1 preadipocytes, characterized by increased ECAR and decreased OCR
*OCR↓,
*p‑AMPK↑, baicalin significantly altered cellular respiration by reducing mitochondrial oxygen consumption while enhancing glycolytic flux, accompanied by increased phosphorylation of AMPK and ACC, suggesting an adaptation to altered energy availability.
*p‑ACC↑,
*Glycolysis↑, significant enrichment in metabolic pathways such as glycolysis, gluconeogenesis, and lipid metabolism.
*lipidDe↓, inhibited the maturation of sterol regulatory element binding protein 1 (SREBP1) and finally alleviated lipid deposition.
*SREBP1↓,
*FAO↑, baicalin induces metabolic reprogramming of adipocytes by inhibiting glucose aerobic metabolism while enhancing anaerobic glycolysis and FAO.
*HK2↑, baicalin upregulated glycolytic enzymes, such as HK1, HK2, PKM2, and LDHA, while downregulating pyruvate dehydrogenase,
*PKM2↑,
*LDHA↑,
*PDKs↓,
*ACC↓, leading to decreased acetyl-CoA production and enhanced fatty acid β-oxidation.
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in-vitro, |
PC, |
NA |
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in-vitro, |
Nor, |
HUVECs |
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in-vivo, |
PC, |
NA |
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tumCV↓,
*toxicity∅, little toxicity on normal cells, e.g, HUVEC cells
TumCMig↓,
TumCI↓,
Apoptosis↑,
AMPK↑,
lipoGen↓,
ACC↓,
FASN↓,
*BioAv↓, Lycopene bioavailability can be decreased by ageing, and some of the pathological states, such as cardiovascular diseases (CVDs)
*AntiCan↑, For instance, it has been shown that a higher dietary intake and circulating concentration of lycopene have protective effects against prostate cancer (PCa), in a dose-dependent way
*ROCK1↓, It remarkably lessened the expression of ROCK1, Ki-67, ICAM-1 and ROCK2,
*Ki-67↓,
*ICAM-1↓,
*cardioP↑, Lycopene is a cardioprotective nutraceutical.
*antiOx↑, Lycopene is a well-known antioxidant.
*NQO1↑, Furthermore, lycopene supplementation improves mRNA expressions of the NQO-1 and HO-1 as antioxidant enzymes.
*HO-1↑,
*TNF-α↓, downregulate inflammatory cytokines (i.e., TNF-α, and IL-1β) in the hippocampus of the mice.
*IL22↓,
*NRF2↑, Lycopene decreased neuronal oxidative damage by activating Nrf2, as well as by inactivating NF-κB translocation in H2O2-related SH-SY5Y cell model
*NF-kB↓,
*MDA↓, significantly reduced the malondialdehyde (MDA)
*Catalase↑, Furthermore, it improved the catalase (CAT), superoxide dismutase (SOD), and GSH levels, and antioxidant capacity [109].
*SOD↑,
*GSH↑,
*cognitive↑, Lycopene administration considerably improved cognitive defects, noticeably reduced MDA levels and elevated GSH-Px activity, and remarkably reduced tau
*tau↓,
*hepatoP↑, Lycopene was also found to be effective against hepatotoxicity by acting as an antioxidant, regulating total glutathione (tGSH) and CAT concentrations
*MMP2↑, It also elevated MMP-2 down-regulation
*AST↓, lowering the liver enzymes levels, like aspartate transaminase (AST), alanine transaminase (ALT), LDL, free fatty acid, and MDA.
*ALAT↓,
*P450↑, Moreover, tomato powder has been shown to have a protective agent against alcohol-induced hepatic injury by inducing cytochrome p450 2E1
*DNAdam↓, lycopene decreased DNA damage
*ROS↓, It has been revealed that they inhibited ROS production, protected antioxidant enzymes, and reversed hepatotoxicity in rats’ liver
*neuroP↑, lycopene consumption relieved cognitive defects, age-related memory loss, neuronal damage, and synaptic dysfunction of the brain.
*memory↑,
*Ca+2↓, Lycopene suppressed the 4-AP-invoked release of glutamate and elevated intra-synaptosomal Ca2+ level.
*Dose↝, an in vivo study revealed that lycopene (6.5 mg/day) was effective against cancer in men [147]. However, lycopene dose should be increased up to 10 mg/day, in the case of advanced PCa.
*Dose↑, lycopene supplementation (15 mg/day, for 12 weeks) in an old aged population improved immune function through increasing natural killer cell activity by 28%
*Dose↝, Finally, according to different epidemiological studies, daily lycopene intake can be suggested to be 2 to 20 mg per day
*toxicity∅, A toxicological study on rats showed the no-observed-adverse-effect level at the highest examined dose (i.e., 1.0% in the diet)
PGE2↓, Lycopene doses of 0, 10, 20, and 30 µM were used to treat human colorectal cancer cell. Prostaglandin E2 (PGE2), and NO levels declined after lycopene administration,
CDK2↓, Treatment with lycopene reduced cell hyperproliferation induced by UVB and ultimately promoted apoptosis and reduced CDK2 and CDK4 complex in SKH-1 hairless mice
CDK4↓,
STAT3↓, lycopene reduced the STAT3 expression in ovarian tissues
NOX↓, (SK-Hep-1) cells and indicated a substantial reduction in NOX activity. Moreover, it inhibits the protein expression of NOX4, NOX4 mRNA and ROS intracellular amounts
NOX4↓,
ROS↓,
*SREBP1↓, Lycopene decreases the fatty acid synthase (FAS), sterol regulatory element-binding protein 1c (SREBP-1c), and Acetyl-CoA carboxylase (ACC1) expression in HFD mice.
*FASN↓,
*ACC↓,
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in-vitro, |
GBM, |
U87MG |
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NA, |
AD, |
NA |
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in-vitro, |
GBM, |
A172 |
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in-vitro, |
GBM, |
T98G |
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Warburg↓, Here, we documented that methylene blue (MB) reverses the Warburg effect evidenced by the increasing of oxygen consumption and reduction of lactate production in GBM cell lines
OCR↑, increases cellular oxygen consumption, and decreases lactate production in murine hippocampal cells
lactateProd↓,
TumCP↓, MB decreases GBM cell proliferation and halts the cell cycle in S phase.
TumCCA↑,
AMPK↑, Through activation of AMP-activated protein kinase, MB inactivates downstream acetyl-CoA carboxylase and decreases cyclin expression.
ACC↓,
Cyc↓,
neuroP↑, There is mounting evidence that MB enhances brain metabolism and exerts neuroprotective effects in multiple neurodegenerative disease models including Parkinson, Alzheimer, and Huntington disease
Cyt‑c↝, MB has long been known as an electron carrier, which is best represented by MB ability to increase the rate of cytochrome c reduction in isolated mitochondria
Glycolysis↓, MB Decreases Aerobic Glycolysis in U87 Cells
ECAR↓, MB increases OCR and decreases ECAR in U87 cells
TumCG↓, MB Inhibits Tumor Growth in Vitro
other↓, MB dramatically inhibits expression of cyclin A2, B1,and D1 while having less effect on cyclin E1
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in-vitro, |
BC, |
MDA-MB-231 |
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TumCP↓,
TumCMig↓,
TumCI↓,
MMP↓,
TLR4↓,
TNF-α↓,
NF-kB↓,
IL1β↓,
IL6↓,
IRAK4↓,
GLUT1↓,
GLUT3↓,
HK2↓,
PFK↓,
PKM2↓,
LDHA↓,
ACC↓,
FASN↓,
eff↓, After adding the glycolysis inhibitor 2-deoxy-D-glucose (2-DG), the inhibitory effects of CAPE on cell viability and migration were not significant when compared with the LPS group.
SREBP1↓, quercetin treatment decreased the immunoreactivities of OGT and SREBP-1 in HeLa cells. Our
TumCP↓, Quercetin decreased cell proliferation and induced cell death, but its effect on HaCaT cells was lower than that on HeLa cells.
TumCD↑,
AMPK↑, Quercetin decreased the expression of global O-GlcNAcylation and increased AMPK activation by reducing the O-GlcNAcylation of AMPK
SREBP1↓, Once activated, AMPK regulates various proteins involved in metabolism, which suppress energy consumption and cellular growth, such as sterol regulatory element binding protein 1 (SREBP-1
FASN↓, FAS and ACC were significantly decreased in cells treated with quercetin
ACC↓,
FASN↓, e sulforaphane (SFaN) impairs fatty acid synthase promoter activity and reduces SREBP target gene (e.g., fatty acid synthase and acetyl-CoA carboxylase 1) expression in human hepatoma Huh-7 cells
ACC↓,
SREBP1↓, SFaN reduced SREBP proteins by promoting the degradation of the SREBP precursor.
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Review, |
Nor, |
NA |
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Review, |
Arthritis, |
NA |
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*hepatoP↑, It improves hepatic function, lessens hepatotoxicity caused by high acetaminophen intake, and can lessen oxidative stress in experimental mice, according to a study on animals
*Inflam↓,
*chemoP↑, moreover reducing the side effect of chemotherapeutic agents.
*glucose↓, Silymarin is effective anti-diabetic as it lowers serum glucose levels thus preventing the development of diabetic nephropathy
*antiOx↑, Various studies revealed that Silymarin could exert antioxidant properties in several mechanisms, which includes direct hindrance in free radical production,
*ROS↓,
*ACC↓, down-regulation of acetyl-CoA carboxylase, fatty acid synthase, and peroxisome proliferator-activated receptor
*FASN↓,
*radioP↑, More studies have revealed radioprotective properties of Silymarin in the testis tissues of mice and rats
*NF-kB↓, Silymarin inhibits NF-kB, down-regulates TGF-ß1 mRNA
*TGF-β↓,
*AST↓, Silymarin significantly decreased the elevation of aspartate aminotransferase (AST), alanine aminotransferase, and alkaline phosphatase in serum, and also reversed the altered expressions of α-smooth muscle actin in fibrotic tissue
*α-SMA↝,
*eff↑, Okda et al.[Citation76] currently reported that silymarin with ginger has significantly decreased the severity and incidence of liver fibrosis.
*neuroP↑, Researchers demonstrated that silymarin inhibits microglia activation, and protects dopaminergic neurons from lipopolysaccharide (LPS)-induced neurotoxicity
eff↑, The Silymarin with a selenium dose of 570 mg/d, for 6 months caused no side effects and was effective in reducing prostate cancer growth
ROS↓, Silymarin shows anti-cancerous properties considered to be linked to oxidative stress inhibition, apoptosis induction, growth cycle arrest, and mitochondrial pathway inhibition
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vitro+vivo, |
Pca, |
LNCaP |
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in-vitro, |
Pca, |
22Rv1 |
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TumCP↓,
Hif1a↓, strongly decreased hypoxia-induced HIF-1α expression
NADPH↓,
angioG↓,
FASN↓,
ACC↓,
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in-vitro, |
Bladder, |
T24/HTB-9 |
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in-vitro, |
Bladder, |
J82 |
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Glycolysis↑, Vitamin K2 renders bladder cancer cells more dependence on glycolysis than TCA cycle
GlucoseCon↑, results suggest that Vitamin K2 is able to induce metabolic stress, including glucose starvation and energy shortage, in bladder cancer cells, upon glucose limitation.
lactateProd↑,
TCA↓, Vitamin K2 promotes glycolysis and inhibits TCA cycle in bladder cancer cells
PI3K↑,
Akt↑,
AMPK↑, Vitamin K2 remarkably activated AMPK pathway
mTORC1↓,
TumAuto↑,
GLUT1↑, Vitamin K2 stepwise elevated the expression of some glycolytic proteins or enzymes, such as GLUT-1, Hexokinase II (HK2), PFKFB2, LDHA and PDHK1, in bladder cancer T24
HK2↑,
LDHA↑, Vitamin K2 stepwise elevated the expression of some glycolytic proteins or enzymes, such as GLUT-1, Hexokinase II (HK2), PFKFB2, LDHA and PDHK1, in bladder cancer T24
ACC↓, Vitamin K2 remarkably decreased the amounts of Acetyl coenzyme A (Acetyl-CoA) in T24 cells
PDH↓, suggesting that Vitamin K2 inactivates PDH
eff↓, Intriguingly, glucose supplementation profoundly abrogated AMPK activation and rescued bladder cancer cells from Vitamin K2-triggered autophagic cell death.
cMyc↓, c-MYC protein level was also significantly reduced in T24 cells following treatment with Vitamin K2 for 18 hours
Hif1a↑, Besides, the increased expression of GLUT-1, HIF-1α, p-AKT and p-AMPK were also detected in Vitamin K2-treated tumor group
p‑Akt↑,
eff↓, 2-DG, 3BP and DCA-induced glycolysis attenuation significantly prevented metabolic stress and rescued bladder cancer cells from Vitamin K2-triggered AMPK-dependent autophagic cell death
eff↓, inhibition of PI3K/AKT and HIF-1α notably attenuated Vitamin K2-upregulated glycolysis, indicating that Vitamin K2 promotes glycolysis in bladder cancer cells via PI3K/AKT and HIF-1α signal pathways.
eff↓, (NAC, a ROS scavenger) not only alleviated Vitamin K2-induced AKT activation and glycolysis promotion, but also significantly suppressed the subsequent AMPK-dependent autophagic cell death.
eff↓, glucose supplementation not only restored c-MYC expression, but also rescued bladder cancer cells from Vitamin K2-triggered AMPK-dependent autophagic cell death
ROS↑, under glucose limited condition, the increased glycolysis inevitably resulted in metabolic stress, which augments ROS accumulation due to lack of glucose for sustained glycolysis.
Showing Research Papers: 1 to 10 of 10
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 10
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
NOX4↓, 1, ROS↓, 2, ROS↑, 1,
Mitochondria & Bioenergetics ⓘ
MMP↓, 1, OCR↑, 1,
Core Metabolism/Glycolysis ⓘ
ACC↓, 7, AMPK↑, 4, cMyc↓, 1, ECAR↓, 1, FASN↓, 5, GlucoseCon↑, 1, Glycolysis↓, 1, 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↓, 3, TCA↓, 1, Warburg↓, 1,
Cell Death ⓘ
Akt↑, 1, p‑Akt↑, 1, Apoptosis↑, 1, Cyt‑c↝, 1, TumCD↑, 1,
Transcription & Epigenetics ⓘ
other↓, 1, tumCV↓, 1,
Autophagy & Lysosomes ⓘ
TumAuto↑, 1,
Cell Cycle & Senescence ⓘ
CDK2↓, 1, CDK4↓, 1, Cyc↓, 1, TumCCA↑, 1,
Proliferation, Differentiation & Cell State ⓘ
mTORC1↓, 1, PI3K↑, 1, STAT3↓, 1, TumCG↓, 1,
Migration ⓘ
TumCI↓, 2, TumCMig↓, 2, TumCP↓, 4,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, Hif1a↓, 1, Hif1a↑, 1,
Barriers & Transport ⓘ
GLUT1↓, 1, GLUT1↑, 1, GLUT3↓, 1,
Immune & Inflammatory Signaling ⓘ
IL1β↓, 1, IL6↓, 1, IRAK4↓, 1, NF-kB↓, 1, PGE2↓, 1, TLR4↓, 1, TNF-α↓, 1,
Cellular Microenvironment ⓘ
NOX↓, 1,
Drug Metabolism & Resistance ⓘ
eff↓, 6, eff↑, 1,
Clinical Biomarkers ⓘ
IL6↓, 1,
Functional Outcomes ⓘ
neuroP↑, 1,
Total Targets: 64
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 2, Catalase↑, 1, GSH↑, 1, HO-1↑, 1, lipidDe↓, 1, MDA↓, 1, NQO1↑, 1, NRF2↑, 1, ROS↓, 2, SOD↑, 1,
Mitochondria & Bioenergetics ⓘ
OCR↓, 1,
Core Metabolism/Glycolysis ⓘ
ACC↓, 3, p‑ACC↑, 1, ALAT↓, 1, p‑AMPK↑, 1, ECAR↑, 1, FAO↑, 1, FASN↓, 2, glucose↓, 1, Glycolysis↑, 1, HK2↑, 1, LDHA↑, 1, PDKs↓, 1, PKM2↑, 1, SREBP1↓, 2,
DNA Damage & Repair ⓘ
DNAdam↓, 1,
Migration ⓘ
Ca+2↓, 1, Ki-67↓, 1, MMP2↑, 1, ROCK1↓, 1, TGF-β↓, 1, α-SMA↝, 1,
Immune & Inflammatory Signaling ⓘ
ICAM-1↓, 1, IL22↓, 1, Inflam↓, 1, NF-kB↓, 2, TNF-α↓, 1,
Synaptic & Neurotransmission ⓘ
tau↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, Dose↑, 1, Dose↝, 2, eff↑, 1, P450↑, 1,
Clinical Biomarkers ⓘ
ALAT↓, 1, AST↓, 2, Ki-67↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, cardioP↑, 1, chemoP↑, 1, cognitive↑, 1, hepatoP↑, 2, memory↑, 1, neuroP↑, 2, radioP↑, 1, toxicity∅, 2,
Total Targets: 55
Scientific Paper Hit Count for: ACC, Acetyl-CoA Carboxylase
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
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