AMPK Cancer Research Results
AMPK, adenosine monophosphate-activated protein kinase: Click to Expand ⟱
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AMPK: guardian of metabolism and mitochondrial homeostasis; Upon changes in the ATP-to-AMP ratio, AMPK is activated. (AMPK) is a key metabolic sensor that is pivotal for the maintenance of cellular energy homeostasis. It is well documented that AMPK possesses a suppressor role in the context of tumor development and progression by modulating the inflammatory and metabolic pathways.
-Activating AMPK can inhibit anabolic processes and the PI3K/Akt/mTOR pathway reducing glycolysis shifting toward Oxidative Phosphorlylation.
AMPK activators:
-metformin or AICAR
-Resveratrol: activate AMPK indirectly
-Berberine
-Quercetin: may stimulate AMPK
-EGCG: thought to activate AMPK
-Curcumin: may activate AMPK
-Ginsenosides: Some ginsenosides have been associated with AMPK activation
-Beta-Lapachone: A natural naphthoquinone compound found in the bark of Tabebuia avellanedae (also known as lapacho or taheebo). It has been observed to activate AMPK in certain models.
-Alpha-Lipoic Acid (ALA): associated with AMPK activation
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Scientific Papers found: Click to Expand⟱
PI3K↝,
AMPK↝,
TumCG↓,
*toxicity↓, No hepatic toxicity found, no weight loss, no hypoglycemia
Weight∅,
*Inflam↓, BBR exerts remarkable anti-inflammatory (94–96), antiviral (97), antioxidant (98), antidiabetic (99), immunosuppressive (100), cardiovascular (101, 102), and neuroprotective (103) activities.
*antiOx↑,
*cardioP↑,
*neuroP↑,
TumCCA↑, BBR could induce G1 cycle arrest in A549 lung cancer cells by decreasing the levels of cyclin D1 and cyclin E1
cycD1/CCND1↓,
cycE/CCNE↓,
CDC2↓, BBR also induced G1 cycle arrest by inhibiting cyclin B1 expression and CDC2 kinase in some cancer cells
AMPK↝, BBR has been suggested to induce autophagy in glioblastoma by targeting the AMP-activated protein kinase (AMPK)/mechanistic target of rapamycin (mTOR)/ULK1 pathway
mTOR↝,
Casp8↑, BBR has been revealed to stimulate apoptosis in leukemia by upregulation of caspase-8 and caspase-9
Casp9↑,
Cyt‑c↑, in skin squamous cell carcinoma A431 cells by increasing cytochrome C levels
TumCMig↓, BBR has been confirmed to inhibit cell migration and invasion by inhibiting the expression of epithelial–mesenchymal transition (EMT)
TumCI↓,
EMT↓,
MMPs↓, metastasis-related proteins, such as matrix metalloproteinases (MMPs) and E-cadherin,
E-cadherin↓,
Telomerase↓, BBR has shown antitumor effects by interacting with microRNAs (125) and inhibiting telomerase activity
*toxicity↓, Numerous studies have revealed that BBR is a safe and effective treatment for CRC
GRP78/BiP↓, Downregulates GRP78
EGFR↓, Downregulates EGFR
CDK4↓, downregulates CDK4, TERT, and TERC
COX2↓, Reduces levels of COX-2/PGE2, phosphorylation of JAK2 and STAT3, and expression of MMP-2/-9.
PGE2↓,
p‑JAK2↓,
p‑STAT3↓,
MMP2↓,
MMP9↓,
GutMicro↑, BBR can inhibit tumor growth through meditation of the intestinal flora and mucosal barrier, and generally and ultimately improve weight loss. BBR has been reported to modulate the composition of intestinal flora and significantly reduce flora divers
eff↝, BBR can regulate the activity of P-glycoprotein (P-gp), and potential drug-drug interactions (DDIs) are observed when BBR is coadministered with P-gp substrates
*BioAv↓, the efficiency of BBR is limited by its low bioavailability due to its poor absorption rate in the gut, low solubility in water, and fast metabolism. Studies have shown that the oral bioavailability of BBR is 0.68% in rats
BioAv↑, combining it with p-gp inhibitors (such as tariquidar and tetrandrine) (196, 198), and modification to berberine organic acid salts (BOAs)
*MAPK↝, Silymarin utilizes a range of molecular mechanisms, including modulation of MAPK, AMPK, NF-κB, mTOR, and PI3K/Akt pathways
*AMPK↝,
*NF-kB↓,
*mTOR↝,
*PI3K↝,
*Akt↝,
*BioAv↝, silymarin faces challenges related to bioavailability and aqueous solubility, hindering its development as a clinical drug
*memory↑, silymarin dose-dependently improves the memory and expression of BDNF in TBI-induced mice along with a significant reduction in the level of glutamate and TNF-α, affirming that silymarin could be a potential therapeutic agent for addressing cognitiv
*BDNF↑,
*TNF-α↓,
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:
Mitochondria & Bioenergetics ⓘ
CDC2↓, 1,
Core Metabolism/Glycolysis ⓘ
AMPK↝, 2,
Cell Death ⓘ
Casp8↑, 1, Casp9↑, 1, Cyt‑c↑, 1, Telomerase↓, 1,
Protein Folding & ER Stress ⓘ
GRP78/BiP↓, 1,
Cell Cycle & Senescence ⓘ
CDK4↓, 1, cycD1/CCND1↓, 1, cycE/CCNE↓, 1, TumCCA↑, 1,
Proliferation, Differentiation & Cell State ⓘ
EMT↓, 1, mTOR↝, 1, PI3K↝, 1, p‑STAT3↓, 1, TumCG↓, 1,
Migration ⓘ
E-cadherin↓, 1, MMP2↓, 1, MMP9↓, 1, MMPs↓, 1, TumCI↓, 1, TumCMig↓, 1,
Angiogenesis & Vasculature ⓘ
EGFR↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, p‑JAK2↓, 1, PGE2↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↑, 1, eff↝, 1,
Clinical Biomarkers ⓘ
EGFR↓, 1, GutMicro↑, 1,
Functional Outcomes ⓘ
Weight∅, 1,
Total Targets: 31
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1,
Core Metabolism/Glycolysis ⓘ
AMPK↝, 1,
Cell Death ⓘ
Akt↝, 1, MAPK↝, 1,
Proliferation, Differentiation & Cell State ⓘ
mTOR↝, 1, PI3K↝, 1,
Immune & Inflammatory Signaling ⓘ
Inflam↓, 1, NF-kB↓, 1, TNF-α↓, 1,
Synaptic & Neurotransmission ⓘ
BDNF↑, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, BioAv↝, 1,
Functional Outcomes ⓘ
cardioP↑, 1, memory↑, 1, neuroP↑, 1, toxicity↓, 2,
Total Targets: 16
Scientific Paper Hit Count for: AMPK, adenosine monophosphate-activated protein kinase
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#:9 State#:% Dir#:4
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