|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
AMPK is generally a tumor suppressor.However, once cancer arises, AMPK becomes a tumor promoter instead, driving cancer development.
|
31787232 |
2020 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The expression levels of miR31, miR92a, KRAS oncogene, and the c-MYC transcription factor were subexpressed upon 72 h post-treatment with kaempferol-3-<i>O</i>-glycoside compared with the control without treatment (<i>P</i> < .05); in contrast, the tumor suppressor genes AMPK (∼4.85, <i>P</i> = .005) and APC (∼2.71, <i>P</i> = .066) tumor suppressors genes were overexpressed.
|
31441682 |
2020 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The signaling pathway activated by metformin (LKB1/AMPK/mTOR) is implicated in tumor suppression in ApcMin/+ mice via metformin-induced reduction in polyp burden, increased ratio of pAMPK/AMPK, decreased pmTOR/mTOR ratio, and decreased pS6Ser235/S6Ser235 ratio in polyps.
|
31818851 |
2020 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In addition, the AMPK activator metformin remarkably suppressed the growth of PCK1-knockout PLC/PRF/5 cells and inhibited tumor growth in an orthotropic HCC mouse model.
|
30717766 |
2019 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Here, we examine the role of AMPK in murine Kras<sup>G12D</sup>-mediated non-small-cell lung cancer (NSCLC), a cancer type in humans that harbors frequent inactivating mutations in the LKB1 tumor suppressor-the predominant upstream activating kinase of AMPK and 12 related kinases.
|
30415923 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
AMPK promotes induction of the tumor suppressor FLCN through activation of TFEB independently of mTOR.
|
31404503 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
CUR/SAL significantly reduces colonic cytokines (p < 0.01), suppresses activation of the PI3K/Akt/mTOR/NF-κB/Wnt pathways (p < 0.01), activates AMPK (p < 0.01), attenuates abnormal proliferation of the colonic mucosa (p < 0.05), and reduces tumor multiplicity and burden (p < 0.05), in comparison to the HFD control.
|
30680927 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Thus, our results demonstrate the primary role of AMPKα1 in the immunosuppressive effects induced by tumor-MDSC and support the therapeutic use of AMPK inhibitors to overcome MDSC-induced T-cell dysfunction in cancer.
|
31409640 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Moreover, in the presence of AMPK activator AMPKinone, the protein level of p-AMPK, p-ULK1, Beclin-1 and LC3-II/LC3-I increased, while the protein expression of p-AMPK, p-ULK1, Beclin-1 and LC3-II/LC3-I decreased in the presence of AMPK inhibitor Compound C. <i>In vivo</i> study using xenograft mice revealed that Zn-CuO NPs significantly inhibited tumor growth with low toxicity.
|
31001120 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
However, whether this is mediated by cell-autonomous AMPK activation within tumor progenitor cells has been unclear.
|
30995468 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Inhibition by fluoxetine of LH-stimulated cyclic AMP synthesis in tumor Leydig cells partly involves AMPK activation.
|
31163038 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Metformin maintained high activation of AMPK and decreased ERK1/2 levels after HF in both cell lines and only after HI in PNT1A, which was able to decrease the cell proliferation triggered by these treatments.
|
29635803 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
AICAR Antiproliferative Properties Involve the AMPK-Independent Activation of the Tumor Suppressors LATS 1 and 2.
|
29730476 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
LKB1-AMPK activation in GC cell lines was tumor suppressive, as metformin (an AMPK activator) inhibited GC cell growth in the CAB39L-silenced cells.
|
30054562 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Metformin inhibited tumor cell proliferation and induced apoptosis through activation of AMPK/mTOR pathway and further influencing energy metabolism, phospholipid metabolism and glucose catabolism.
|
29705631 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
AMPK activation, RTK degradation, and Akt inhibition were observed in itraconazole-treated tumors.
|
29592879 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Tumour suppression correlated with 37.6- and 18.9-fold increases in plasma and tumour BCAAs, 37.5% and 30.4% decreases in tumour glutamine and alanine, and a 3.5-fold increase in the phosphorylation of tumour AMPK in BCATmKO mice on standard rodent chow.
|
30318512 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
NDV can function as a tumor cell selective approach to inhibit AKT and activate AMPK.
|
30065314 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The xenograft mouse model further confirmed that metformin inhibited tumor growth by upregulation of AMPK and downregulation of mTOR.
|
29554968 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Altogether, our data identified Mst1 as a novel tumor-suppressive factor in promoting cell death in gastric cancer cells by triggering mitochondrial fission and blocking the AMPK-Sirt3 axis.
|
30555239 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Western blot analysis and confocal microscopy results indicated that overexpression of miR-138 or interference of Sirt1 expression could inhibit lung cancer cell autophagy activity possibly through AMPK-mTOR signaling pathway. miR-138 plays a tumor suppressor function in lung cancer.
|
28498463 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In this work, we report our three leading research qualities: (1) CPPA hybrid microspheres with hollow and porous structure are synthesized by a facile one-step microwave-assisted solvothermal method; (2) CPPA hybrid microspheres show high doxorubicin loading capacity and pH-responsive drug release properties, and demonstrate positive therapeutic effects on six osteosarcoma cell lines in vitro and a mouse model of 143B osteosarcoma subcutaneous tumor in vivo; (3) CPPA hybrid microspheres are favorable to promote osteogenic differentiation of human bone mesenchymal stem cells (hBMSCs) by activating the AMPK pathway, with satisfactory evidences from cellular alkaline phosphatase staining, alizarin red staining, real time PCR and western analysis.
|
28063979 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Two-thirds of existing mammary tumors responded to metformin treatment with decreased tumor volumes (<i>P</i> < 0.05), reduced proliferative index (<i>P</i> < 0.01), and activated AMPK (<i>P</i> < 0.05).
|
28154203 |
2017 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The molecular mechanisms involved in fenofibrate's ability to delay tumor development included the down-regulation of mTOR activity via TSC1/2-dependent signaling through activation of AMPK and inactivation of Akt, or via a TSC1/2-independent pathway through direct suppression of raptor.
|
27313493 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Bmi-1 is a transcriptional regulator that promotes tumor cell self-renewal and epithelial to mesenchymal transition and its upregulation is associated with tumor progression, AMPK is an intracellular fuel-sensing enzyme and plays important roles in tumor cell growth and progression.
|
26717043 |
2016 |