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AKT decreases the amount of MYC. 20 / 21
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"These data suggest that metformin controls cellular hyperproliferation in AKT/c-Met mice by limiting ERK phosphorylation and c-Myc and cyclin D1 expression.HCC is a commonly occurring malignancy with [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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

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"It is plausible that AKT and ERK inactivation may have reduced the expression of mTOR and c-Myc, resulting in the downregulation of HIF-1α and GLUT1 expression in the present study."

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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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"Herein, we observed a significant decrease expression level of total PI3K-p85, p-PI3K-p85, total Akt, p-Akt, GSK-3β and p-GSK-3β, as well as their downstream, β-catenin, c-Myc and cyclin D1 after treatment with Chr-A at different concentrations for 48 h in U251 and U87-MG cells, suggesting that Chr-A could downregulate PI3K-activated Akt followed by downregulation of GSK-3β, thus attenuating expression of β-catenin and downstream, c-Myc, cyclin D1, slug, MMP2 and MMP9 to inhibit proliferation and the EMT process of human glioblastoma cells."

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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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"This result, that Akt reduces c- myc expression, is consistent with results using an inducible form of the kinase in NIH 3T3 cells [49] , and given the role of c-Myc in apoptosis, is consistent with t[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Even if glutamine metabolism was not investigated, downregulation of activated AKT was shown to reduce the level of c-MYC and prevent tumor cell growth ( Quan et al., 2015 )."

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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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"Furthermore, consistent with in vivo findings, the protein expression of Cyclin D1 and c-Myc was suppressed by celecoxib incubation in the AKT/c-Met overexpressing cells (Fig. 4E and F)."

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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."

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"Interestingly, this miR-181a mediated inhibition of AKT activation increased c-MYC expression, further upregulating miR-181a, and establishing a miR-181a-5p-TCL1A-AKT/mTOR-c-MYC feedback loop."

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"We found that inhibiting AKT with MK-2206 attenuated Sema3C-mediated stemness and reduced Gli1 and c-Myc expression, providing new evidence that Sema3C functions via the AKT/Gli1/c-Myc axis in HCC cells.In general, as a secreted protein, Sema3C needs to bind to receptors on the cell surface to perform specific functions."

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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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"Akt activator also impaired the inhibition of the protein expression of total β-catenin, p-β-catenin, active β-catenin, c-Myc, and Cyclin D1 resulting from CD58 depletion (Fig. 7d)."

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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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"AKT inhibits GSK3β, increasing cMyc protein levels and stability."

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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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"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."