|
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 |
In order to address this multi-scale nature of glioblastoma proliferation and invasion and its response to conventional treatment, we propose a hybrid model of glioblastoma that analyses spatio-temporal dynamics at the cellular level, linking individual tumor cells with the macroscopic behaviour of cell organization and the microenvironment, and with the intracellular dynamics of miR-451-AMPK-mTOR signaling within a tumour cell.
|
25629604 |
2015 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Thus, AMPK-α1 can be a cell-autonomous tumor suppressor in the context of T-ALL, and phenformin may have potential for the prevention of some cancers.
|
30995468 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
New work from the Alessi laboratory in this issue of the Biochemical Journal shows conclusively that AMPK activators delay the growth of tumours that occur spontaneously in PTEN (phosphatase and tensin homologue deleted on chromosome 10) heterozygous mice.
|
18466113 |
2008 |
|
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 |
GeneticVariation
|
group |
BEFREE |
Our meta-analysis showed that AMPK pathway had significant associations with progression-free survival (PFS; p < 0.001) and overall survival (OS; p < 0.001), but not with tumor response (TR; p = 0.220): PRKAA1 rs13361707 was significantly associated with favorable PFS (log HR = -0.219, SE = 0.073, p = 0.003), as well as PRKAA1 rs10074991 (log HR = -0.215, SE = 0.073, p = 0.003), and there were suggestive associations of PRKAG1 rs1138908 with unfavorable OS (log HR = 0.170, SE = 0.083, p = 0.041), and of UBE2O rs3803739 with unfavorable PFS (log HR = 0.137, SE = 0.068, p = 0.042) and OS (log HR = 0.210, SE = 0.077, p = 0.006), although these results were not significant after false discovery rate adjustment.
|
30856283 |
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 |
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 |
It was yet ineffective against AMPKα1 shRNA-expressing Eca-109 tumors.
|
29592879 |
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 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 |
AlteredExpression
|
group |
BEFREE |
High levels of RNF44 corresponding to low levels of AMPK-α1 appeared in BR xenografts and melanoma tumor samples from BR and BRAFi/MEK inhibitor (MEKi)-resistant (BMR) melanoma patients.
|
29094484 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Yet, its anti-tumor activity was significantly weakened against AMPKα1-silenced HCT-116 tumors.
|
28407688 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Cell proliferation and oncogenic assays demonstrate that PIKE-A antagonizes tumor suppressive actions of AMPK.
|
26001218 |
2016 |
|
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 |
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 |
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 |
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 |
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 |
We concluded that CYC1 promoted tumor metastasis via suppressing activation of AMPK and contributed to tumor growth via facilitating production of ATP.
|
27239088 |
2016 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Using RT-PCR, PRKAA1 mRNA expression in seven tumor samples with known 5p amplification was amplified from 3- to 15-fold.
|
16595147 |
2006 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Mechanistically, C19 induced GSK3-β-mediated degradation of the Hippo transducer TAZ, through activation of the Hippo kinases Mst/Lats and the tumor suppressor kinase AMPK upstream of the degradation complex.
|
24694946 |
2014 |
|
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 |
AlteredExpression
|
group |
BEFREE |
We suggest that these tumours may arise through a mechanism involving ATP depletion, activation of AMPK, and induction of cyclin D1, and that this may be a unique pathway of tumour development that has the potential for therapeutic intervention in these rare tumours.
|
24236567 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Our study suggests that the two isoforms of AMPKα, AMPKα1 and AMPKα2 play different roles in controlling tumour development.
|
30636376 |
2019 |