IndraLab

Statements


AKT decreases the amount of MYC. 10 / 11
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"If mTORC2 dependent FoxO acetylation maintains c-Myc levels to drive PI3K or Akt inhibitor resistance, then combined suppression of mTORC2, and PI3K or Akt should decrease cellular levels of c-Myc, potentially causing tumor cell death."

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"Indeed, AKT inhibition by AZD5363 diminished phosphorylation of GSK3beta, a direct downstream target of AKT, and reduced expression of both MYC and PRMT5 in all six cell lines (XREF_FIG, left panel)."

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"39 Furthermore, c-Myc is upregulated by Akt, the suppression of which inhibits c-Myc expression."

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"Notably, inhibition of glycolysis effectively killed sensitive and resistant leukaemia cells and potently restored the sensitivity of MDR cells to the anticancer agent ADM. The AKT serine/threonine kinase (AKT)/mechanistic target of rapamycin (mTOR) signalling pathway, a crucial regulator of glycometabolic homeostasis, mediated over-activation and upregulation of c-Myc expression levels in K562 and ADM cells, which directly stimulated glucose consumption and enhanced glycolysis."

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"Consequently, PKB mediated phosphorylation and inhibition of GSK3 activity will increase cyclin D, cyclin E and c-MYC expression."

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"Interruption of AKT pathway suppressed the expression of NF-kappaB and c-Myc, furthermore, the expression of a set of miRNAs was also changed after AKT siRNA transfection."

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"In addition, SET knockdown mediated dephosphorylation of Akt downregulated the expression of c-Myc and Cyclin D1, which inhibited the cell survival in CRC."

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"Additionally, the SYK dependent activation of AKT and consequent inhibition of GSK3 increases the intracellular level of MYC, whose degradation is enhanced when phosphorylated by GSK3."

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"Collectively, these results indicate that inhibition of the HER2 and AKT pathway in multiple breast cancer cell lines induces expression of c-Myc."

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"Consistently, our results showed that inhibition of Akt via ectopic expression of AKT-DN induces a moderate increase in c-Myc and miR-9-3p expression, indicating a possible role of Akt in preventing c-Myc-miR-9-3p activation."