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⟱
*AChE↓, ALA activated AChE and increased glucose uptake, thus providing more acetyl-CoA to generate acetylcholine (ACh). (note activated AChE in this review likely should say inhibited!!!)
*GlucoseCon↑,
*ACC↑,
*GSH↑, ALA increased intracellular GSH levels by chelating redox-active transition metals, thus inhibiting the formation of hydroxyl radicals and Aβ aggregation.
*Aβ↓,
*Catalase↑, Levels of several antioxidant enzymes including catalase, GR, glutathione-S-transferase (GST), NADPH, and quinone oxidoreductase-1 (NQO1) were enhanced by ALA
*GSR↑,
*GSTs↑,
*NADPH↑,
*NQO1↑,
*iNOS↓, LA prevented the induction of iNOS, inhibited TNFα-induced activation of NF-κB [42], levels of which are
increased in AD.
*NF-kB↓,
*lipid-P↓, ALA reduced the levels of lipid peroxidation products
*BBB↑, ALA could
easily cross the blood–brain barrier (BBB)
*memory↑, ALA treatment significantly improved the spatial memory and cognition capacity of the mice in the Morris
water maze and novel object recognition test.
*cognitive↑,
*antiOx↑, antioxidant and anti-inflammatory activities of ALA
*Inflam↓,
*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/SREBF1↓,
*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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vitro+vivo, |
CRC, |
HCT116 |
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in-vitro, |
CRC, |
SW480 |
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in-vitro, |
CRC, |
LoVo |
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TumVol↓, berberine treated mice showed a 60% reduction in tumor number
Ki-67↓, Berberine also decreased AOM/DSS induced Ki-67 and COX-2 expression
COX2/PTGS2↓,
AMPK↑, Berberine activated AMP-activated protein kinase (AMPK), a major regulator of metabolic pathways, and inhibited mammalian target of rapamycin (mTOR),
mTOR↓, Berberine Inhibits mTOR Signaling in CRC Cells
NF-kB↓, Berberine inhibited Nuclear Factor kappa-B (NF-κB) activity, reduced the expression of cyclin D1 and survivin, induced phosphorylation of p53 and increased caspase-3 cleavage in vitro.
cycD1/CCND1↓,
survivin↓,
P53↑,
cl‑Casp3↑,
TumCP↓, berberine suppresses colon epithelial proliferation and tumorigenesis via AMPK dependent inhibition of mTOR activity and AMPK independent inhibition of NF-κB.
Inflam↓, Berberine Inhibits AOM/DSS-induced Inflammation and Proliferation
COX2/PTGS2↓, We found COX-2 expression to be significantly decreased in berberine treated animals on day 70
ACC↑, Berberine Activates AMPK and Acetyl-CoA Carboxylase (ACC) in CRC Cells
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in-vitro, |
HCC, |
HepG2 |
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in-vitro, |
HCC, |
HUH7 |
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ChemoSen↑, combination treatment using capsaicin and sorafenib, increased apoptosis, followed by the activation of caspase-9 and PARP, was observed.
Apoptosis↑,
Casp9↑,
PARP↑,
Akt↓, sorafenib treatment induces activation of Akt, probably as a mechanism of resistance, whereas capsaicin inhibits Akt
AMPK↑, combination of capsaicin and sorafenib induce AMPK activation and Acetyl CoA carboxylase phosphorylation in HCC cells.
p‑ACC↑,
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in-vitro, |
Melanoma, |
U266 |
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TumCD↑, Fisetin elicited the cytotoxicity in U266 cells, manifested as an increased fraction of the cells with sub-G1 content or stained positively with TUNEL labeling
TumCCA↑,
Casp3↑, Fisetin enhanced caspase-3 activation, downregulation of Bcl-2 and Mcl-1L, and upregulation of Bax, Bim and Bad
Bcl-2↓,
Mcl-1↓,
BAX↑,
BIM↑,
BAD↑,
AMPK↑, Fisetin activated AMPK as well as its substrate acetyl-CoA carboxylase (ACC), along with a decreased phosphorylation of AKT and mTOR.
ACC↑,
p‑Akt↓,
p‑mTOR↓,
ROS↑, Fisetin also stimulated generation of ROS in U266 cells
eff↓, Conversely, compound C or N-acetyl-l-cystein blocked fisetin-induced apoptosis
COX2/PTGS2↓, fisetin altered the expression of cyclooxygenase 2 (COX2) thereby suppressed the secretion of prostaglandin E2 ultimately resulting in the inhibition of epidermal growth factor receptor (EGFR) and NF-κB in human colon cancer cells HT29
PGE2↓,
EGFR↓,
Wnt↓, fisetin treatment inhibited the stimulation of Wnt signaling pathway via downregulating the expression of β-catenin and Tcell factor (TCF) 4
β-catenin/ZEB1↓,
TCF↑,
Apoptosis↑, fisetin triggers apoptosis in U266 cells through multiple pathways: enhancing the activation of caspase-3 and PARP cleavage, decreasing the expression of anti-apoptotic proteins (Bcl-2 and Mcl-1 L ),
Casp3↑,
cl‑PARP↑,
Bcl-2↓,
Mcl-1↓,
BAX↑, ncreasing the expression of pro-apoptotic proteins (Bax, Bim, and Bad)
BIM↑,
BAD↑,
Akt↓, decreasing the phosphorylation of AKT and mTOR and elevating the expression of acetyl CoA carboxylase (ACC
mTOR↓,
ACC↑,
Cyt‑c↑, release the cytochrome c and Smac/Diablo into the cytosol
Diablo↑,
cl‑Casp8↑, fisetin exhibited an increased level of cleaved caspase-8, Fas/Fas ligand, death receptor 5/TRAIL, and p53 levels in HCT-116 cells
Fas↑,
DR5↑,
TRAIL↑,
Securin↓, Securin gets degraded on exposure to fisetin in colon cancer cells.
CDC2↓, fisetin decreased the expression of cell division cycle proteins (CDC2 and CDC25C)
CDC25↓,
HSP70/HSPA5↓, Fisetin induced apoptosis as a result of the downregulation of HSP70 and BAG3 and the inhibition of Bcl-2, Bcl-x L and Mcl-1. T
CDK2↓, AGS 0, 25, 50, 75 μM – 24 and 48 h ↓CDK2, ↓CDK4, ↓cyclin D1, ↑casapse-3 cleavage
CDK4↓,
cycD1/CCND1↓,
MMP2↓, A549 0, 1, 5, 10 μM- 24 and 48 hr: ↓MMP-2, ↓u-PA, ↓NF- κB, ↓c-Fos, ↓c-Jun
uPA↓,
NF-kB↓,
cFos↓,
cJun↓,
MEK↓, ↓ MEK1/2 and ERK1/2 phosphorylation, ↓N-cadherin, ↓vimentin, ↓snail, ↓fibronectin, ↑E-cadherin, ↑desmoglein
p‑ERK↓,
N-cadherin↓,
Vim↓,
Snail↓,
Fibronectin↓,
E-cadherin↓,
NF-kB↑, increased expression of NF-κB p65 leading to apoptosis was due to ROS generation on exposure to fisetin
ROS↑,
DNAdam↑, increased ROS triggered cell death through PARP cleavage, DNA damage and mitochondrial membrane depolarization.
MMP↓,
CHOP/DDIT3↑, Though fisetin upregulated CHOP expression and increased the production of ROS, these events fail to induce apoptosis in Caki cells.
eff↑, 50 μM fisetin + 1 mM melatonin Sk-mel-28 Enhances anti-tumour activity [54]
20 μM fisetin + 1 mM melatonin MeWo Enhances anti-tumour activity [54]
10 μM fisetin + 0.1 μM melatonin A549 Induces autophagic cell death
ChemoSen↑, 20 μM fisetin + 5 μM sorafenib A375, SK-MEL-28 Suppresses invasion and metastasis [44]
40 μM fisetin + 10 μM cisplatin A549, A549-CR Enhances apoptosis
PI3K↓, block multiple signaling pathways such as the phosphatidylinositol-3-kinase/protein kinase
B/mammalian target of rapamycin (PI3K/Akt/mTOR) and p38
Akt↓,
mTOR↓,
p38↓,
*antiOx↑, antioxidant, anti-inflammatory, antiangiogenic, hypolipidemic, neuroprotective, and antitumor effect
*neuroP↑,
Casp3↑, U266 cancer cell line through activation of caspase-3, downregulation of Bcl-2 and Mcl-1L, upregulation of Bax, Bim and Bad
Bcl-2↓,
Mcl-1↓,
BAX↑,
BIM↑,
BAD↑,
AMPK↑, activation of 5'adenosine monophosphate-activated protein kinase (AMPK), acetyl-CoA carboxylase (ACC) and decreased phosphorylation of AKT and mTOR were also observed
ACC↑,
DNAdam↑, DNA fragmentation, mitochondrial membrane depolarizatio
MMP↓,
eff↑, fisetin in combination with a citrus flavanone, hesperetin mediated apoptosis by
mitochondrial membrane depolarization and caspase-3 act
ROS↑, NCI-H460 human non-small cell lung cancer line, fisetin generated reactive oxygen species (ROS), endoplasmic reticulum (ER) stress
cl‑PARP↑, fisetin treatment resulted in PARP cleavage
Cyt‑c↑, release of cyt. c
Diablo↑, release of cyt. c and Smac/DIABLO from mitochondria,
P53↑, increased p53 protein levels
p65↓, reduced phospho-p65 and Myc oncogene expression
Myc↓,
HSP70/HSPA5↓, fisetin causes inhibition of proliferation by the modulation of heat shock protein 70 (HSP70), HSP27
HSP27↓,
COX2/PTGS2↓, anti-proliferative effects of fisetin through the activation of apoptosis via inhibition of cyclooxygenase-2 (COX-2) and Wnt/EGFR/NF-κB signaling pathways
Wnt↓,
EGFR↓,
NF-kB↓,
TumCCA↑, The anti-proliferative effects of fisetin and hesperetin were shown to be occurred through S, G2/M, and G0/G1 phase arrest in K562 cell progression
CDK2↓, decrease in levels of cyclin D1, cyclin A, Cdk-4 and Cdk-2
CDK4↓,
cycD1/CCND1↓,
cycA1/CCNA1↓,
P21↑, increase in p21
CIP1/WAF1
levels in HT-29 human colon cancer cell
MMP2↓, fisetin has exhibited tumor inhibitory effects by blocking matrix metalloproteinase-2 (MMP- 2) and MMP-9 at mRNA and protein levels,
MMP9↓,
TumMeta↓, Antimetastasis
MMP1↓, fisetin also inhibited the MMP-14,
MMP-1, MMP-3, MMP-7, and MMP-9
MMP3↓,
MMP7↓,
MET↓, promotion of mesenchymal to epithelial transition associated with a decrease in mesenchymal markers i.e. N-cadherin, vimentin, snail and fibronectin and an increase in epithelial markers i.e. E-cadherin
N-cadherin↓,
Vim↓,
Snail↓,
Fibronectin↓,
E-cadherin↑,
uPA↓, fisetin suppressed the expression and activity of urokinase plasminogen activator (uPA)
ChemoSen↑, combination treatment of fisetin and sorafenib reduced the migration and invasion of BRAF-mutated melanoma cells both in in-vitro
EMT↓, inhibited epithelial to mesenchymal transition (EMT) as observed by a decrease in N-cadherin, vimentin and fibronectin and an increase in E-cadherin
Twist↓, inhibited expression of Snail1, Twist1, Slug, ZEB1 and MMP-2 and MMP-9
Zeb1↓,
cFos↓, significant decrease in NF-κB, c-Fos, and c-Jun levels
cJun↓,
EGF↓, Fisetin inhibited epidermal growth factor (EGF)
angioG↓, Antiangiogenesis
VEGF↓, decreased expression of endothelial nitric oxide synthase
(eNOS) and VEGF, EGFR, COX-2
eNOS↓,
*NRF2↑, significantly increased nuclear translocation of Nrf2 and antioxidant response element (ARE) luciferase activity, leading to upregulation of HO-1 expression
HO-1↑,
NRF2↓, Fisetin also triggered the suppression of Nrf2
GSTs↓, declined placental type glutathione S-transferase (GST-p) level in the liver of the fisetin- treated rats with hepatocellular carcinoma (HCC)
ATF4↓, Fisetin also rapidly increased the levels of both Nrf2 and ATF4
*antiOx↑, Isoquercitrin, a flavonoid glycoside found in various plants, has demonstrated antioxidant, anti-inflammatory, and anticancer properties
*Inflam↓,
*AntiCan↑,
*ROS↓, HepG2 cells exposed to arachidonic acid (AA) and iron exhibited oxidative stress-induced apoptosis, which was significantly attenuated by isoquercitrin treatment
*MMP↑, Isoquercitrin decreased reactive oxygen species (ROS) generation and preserved mitochondrial function in a dose-dependent manner.
*STK11/LKB1↑, isoquercitrin activates the LKB1/AMPK pathway, increasing phosphorylation of AMPK and its downstream target ACC, thereby modulating energy metabolism and reducing oxidative stress.
*AMPK↑,
*p‑AMPK↑,
*ACC↑,
*ALAT↓, isoquercitrin protected mice against carbon tetrachloride-induced liver injury, reducing serum ALT and AST levels and improving histopathological features.
*AST↓,
*hepatoP↑, isoquercitrin exerts hepatoprotective effects by activating the LKB1/AMPK pathway and modulating metabolic enzymes, highlighting its potential as a therapeutic agent against oxidative liver damage.
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in-vitro, |
HCC, |
HepG2 |
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in-vitro, |
HCC, |
SK-HEP-1 |
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lipidLev↓, Though lambertianic acid (LA) is reported to have hypolipidemic activity in liver
TumCCA↑, LA increased cytotoxicity, sub-G1 population and Annexin V/PI positive cells in two HCC cells
cl‑Casp3↑, LA cleaved caspase-3 and poly(ADP-ribose) polymerase (PARP), activated phosphorylation of liver kinase B1 (LKB1)/AMP activated protein kinase (AMPK)/ acetyl-CoA carboxylase (ACC) pathway
cl‑PARP↑,
AMPK↑,
Akt↓, also suppressed antiapoptotic proteins such as phosphorylation of Akt/ mammalian target of rapamycin (mTOR) and the expression of B cell lymphoma-2 (Bcl-2)/ B-cell lymphoma-extra large (Bcl-xL) and cyclooxygenase-2 (COX-2) in two HCC cells.
mTOR↓,
Bcl-2↓,
Bcl-xL↓,
COX2/PTGS2↓,
ROS↑, LA generated reactive oxygen species (ROS) in HepG2 cells
eff↓, AMPK inhibitor compound C or ROS inhibitor N-acetyl-L-cysteine (NAC) blocked the apoptotic ability of LA to cleave PARP or increase sub G1 population in HepG2 cells.
p‑STK11/LKB1↑, Overall, these findings suggest that ROS dependent phosphorylation of LKB1/AMPK/ACC signaling is critically involved in LA induced apoptosis in HCCs.
p‑ACC↑,
*Obesity↓, labmertianic acid (LA) is known to have anti-obesity [40], stress-protective [41], anti-allergic [42] and neurotropic
*Stress↓,
*antiAll↑,
tumCV↓, LA significantly suppressed the viability of HepG2, SK-Hep1 and Hep3B cells in a concentration dependent fashion, but not Chang normal hepatocyte cells.
selectivity↑,
TumCP↓, LA significantly inhibited proliferation of two HCC cells in a concentration and time dependent manner
*Obesity↓, potential health benefits in attenuating obesity, allergies and different cancers including breast, liver, lung and prostate cancer.
*AntiCan↑,
*AMPK↑, rats with high fat diet (HFD)-induced obesity by activating adenosine monophosphate activated protein kinase (AMPK)
*β-HEX↓, it was also observed that LA can suppress the release of β-hexosaminidase in a concentration-independent manner in BMMC
NA↑, anti-allergic activity
TumCCA↑, LA-treated MDA-MB-231 cells revealed that LA induces G2/ M phase arrest
AMPK↑, , LA activates AMPK and acetyl-CoA carboxylase (ACC) through phosphorylation and can suppress protein kinase B (AKT) phosphorylation,
ACC↑,
p‑Akt↓,
FOXM1↓, LA actively attenuates the expression of forkhead box protein M1 (FOXM1) and its regulated gene products, including proliferative proteins (Cyclin B1) and anti-apoptotic proteins (X-linked inhibitor of apoptosis protein [XIAP] and B-cell lymphoma 2 [
CycB/CCNB1↓,
XIAP↓,
Bcl-2↓,
p‑STAT3↓, LA suppresses the phosphorylation of STAT3 and NF-κB, the expression of p300 and RelA/ p65 acetylation,
p‑NF-kB↓,
Bcl-xL↓, LA blocks the expression of NF-κB regulated genes, including anti-apoptotic proteins (Bcl-2, Bcl-xL, XIAP and survivin), angiogenic protein vascular endothelial growth factor (VEGF), inflammatory protein COX-2, oncogenic genes cellular myelocytomato
survivin↓,
VEGF↓,
COX2/PTGS2↓,
cMyc↓,
IL6↓, and inflammatory mediators IL-6 and tumour necrosis factor-alpha (TNF-α) in the MCF-7 cells
TNF-α↓,
ROS↑, LA exhibits anticancer effects on hepatocellular carcinoma cells (HCC) through induction of apoptotic pathway by ROS-dependent activation of liver kinase B1 (LKB1)/AMPK/ ACC signalling cascades
STK11/LKB1↑,
cl‑Casp3↑, it induces the cleavage of caspase-3 and PARP along with the suppression of antiapoptotic proteins, Bcl-2 and Bcl-xl.
cl‑PARP↑,
eff↑, LA (20 μM) together with TRAIL (20 ng/ml) shows significant cytocidal effects in TRAIL resistant nonsmall cell lung cancer cell
AR↓, LA exerts anticancer effects by suppressing AR pathway in AR-sensitive prostate cancer cells LNCaP.
TumCP↓, 24 h LA treatment downregulates cell proliferation by reducing several protein levels, including p-53, p-p53, p21, p27, cyclin D1 and cell division kinase 4 (CDK4).
p‑P53↓,
P21↓,
p27/CDKN1B↓,
cycD1/CCND1↓,
CDK4↓,
PSA↓, LA exhibits anticancer properties by inhibiting AR expression and PSA in cellular and secretory levels
STAT3↓, LA induces apoptosis via miRNA-134 mediated inhibition of STAT3 and RelA/p65 acetylation
ac‑p65↓,
*antiAll↑, In conclusion, LA could be utilized in treating allergies, obesity and different cancers.
SIRT1↑, Mechanistically, high-dose NMN promotes ferroptosis through NAM-mediated SIRT1–AMPK–ACC signaling
Dose↝, At low doses (10 and 20 mM) and prolonged exposure (48 h), NMN increased cell proliferation, but it induced the suppression of cell proliferation at the high dose (100 mM)
TumCP⇅,
Ferroptosis↑, High-Dosage NMN Inhibits Lung Cancer Growth by Inducing Ferroptosis Program
lipid-P↑, high-dose NMN increased lipid peroxide accumulation in the A549 and SPCA1 cells.
AMPK↑, high-dose NMN treatment can activate SIRT1–AMPK–ACC signaling mediated through an overload of NAM.
ACC↑,
*OXPHOS↑, suggesting that OXPHOS activity is needed for maximal inhibition of M1 marker expression by Sfn
*M1↓,
*IL1β↓, Consistent with our previous study [40], presence of Sfn significantly diminished mRNA expression of il1β, il6, nos2, and tnfα in M1 (LPS) cells
*IL6↓,
*NOS2↓,
*TNF-α↓,
*ROS↓, 0 and 10 μM, impaired M1 marker expression, ROS or NO production and preserved respiratory activity after LPS exposure
*NO↓,
*ACC↑, Sfn prevents the drop of nuclear and cytosolic acetyl-CoA in LPS-stimulated macrophages
Showing Research Papers: 1 to 12 of 12
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
NA↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
Ferroptosis↑, 1, GSTs↓, 1, HO-1↑, 1, lipid-P↑, 1, NRF2↓, 1, ROS↑, 5,
Mitochondria & Bioenergetics(tgid=3) ⓘ
CDC2↓, 1, CDC25↓, 1, EGF↓, 1, MEK↓, 1, MMP↓, 2, XIAP↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ACC↑, 6, p‑ACC↑, 2, AMPK↑, 7, cMyc↓, 1, lipidLev↓, 1, SIRT1↑, 1, STK11/LKB1↑, 1, p‑STK11/LKB1↑, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 4, p‑Akt↓, 2, Apoptosis↑, 2, BAD↑, 3, BAX↑, 3, Bcl-2↓, 5, Bcl-xL↓, 2, BIM↑, 3, Casp3↑, 3, cl‑Casp3↑, 3, cl‑Casp8↑, 1, Casp9↑, 1, Cyt‑c↑, 2, Diablo↑, 2, DR5↑, 1, Fas↑, 1, Ferroptosis↑, 1, Mcl-1↓, 3, Myc↓, 1, p27/CDKN1B↓, 1, p38↓, 1, survivin↓, 2, TRAIL↑, 1, TumCD↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
cJun↓, 2, tumCV↓, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP/DDIT3↑, 1, HSP27↓, 1, HSP70/HSPA5↓, 2,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↑, 2, P53↑, 2, p‑P53↓, 1, PARP↑, 1, cl‑PARP↑, 4,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK2↓, 2, CDK4↓, 3, cycA1/CCNA1↓, 1, CycB/CCNB1↓, 1, cycD1/CCND1↓, 4, P21↓, 1, P21↑, 1, Securin↓, 1, TumCCA↑, 4,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
cFos↓, 2, EMT↓, 1, p‑ERK↓, 1, FOXM1↓, 1, mTOR↓, 4, p‑mTOR↓, 1, PI3K↓, 1, STAT3↓, 1, p‑STAT3↓, 1, TCF↑, 1, Wnt↓, 2,
Migration(tgid=13) ⓘ
E-cadherin↓, 1, E-cadherin↑, 1, Fibronectin↓, 2, Ki-67↓, 1, MET↓, 1, MMP1↓, 1, MMP2↓, 2, MMP3↓, 1, MMP7↓, 1, MMP9↓, 1, N-cadherin↓, 2, Snail↓, 2, TumCP↓, 3, TumCP⇅, 1, TumMeta↓, 1, Twist↓, 1, uPA↓, 2, Vim↓, 2, Zeb1↓, 1, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 1, ATF4↓, 1, EGFR↓, 2, eNOS↓, 1, VEGF↓, 2,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 6, IL6↓, 1, Inflam↓, 1, NF-kB↓, 3, NF-kB↑, 1, p‑NF-kB↓, 1, p65↓, 1, ac‑p65↓, 1, PGE2↓, 1, PSA↓, 1, TNF-α↓, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
AR↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
ChemoSen↑, 3, Dose↝, 1, eff↓, 2, eff↑, 3, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
AR↓, 1, EGFR↓, 2, FOXM1↓, 1, IL6↓, 1, Ki-67↓, 1, Myc↓, 1, PSA↓, 1,
Functional Outcomes(tgid=23) ⓘ
TumVol↓, 1,
Total Targets: 125
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
antiAll↑, 2, Stress↓, 1, β-HEX↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 3, Catalase↑, 1, GSH↑, 1, GSR↑, 1, GSTs↑, 1, lipid-P↓, 1, lipidDe↓, 1, NQO1↑, 1, NRF2↑, 1, OXPHOS↑, 1, ROS↓, 2,
Mitochondria & Bioenergetics(tgid=3) ⓘ
MMP↑, 1, OCR↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ACC↓, 1, ACC↑, 3, p‑ACC↑, 1, ALAT↓, 1, AMPK↑, 2, p‑AMPK↑, 2, ECAR↑, 1, FAO↑, 1, GlucoseCon↑, 1, Glycolysis↑, 1, HK2↑, 1, LDHA↑, 1, NADPH↑, 1, PDKs↓, 1, PKM2↑, 1, SREBP1/SREBF1↓, 1, STK11/LKB1↑, 1,
Cell Death(tgid=5) ⓘ
iNOS↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
NO↓, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
IL1β↓, 1, IL6↓, 1, Inflam↓, 2, M1↓, 1, NF-kB↓, 1, TNF-α↓, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
AChE↓, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, AST↓, 1, IL6↓, 1, NOS2↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 2, cognitive↑, 1, hepatoP↑, 1, memory↑, 1, neuroP↑, 1, Obesity↓, 2,
Total Targets: 54
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
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:% Target#:932 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
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