Study data from human hepatocellular carcinoma (HCC) liver samples human HCC cells and Sgk3 knockout mice model suggest that SGK3 plays a role in transducing helical domain mutant PIK3CA signaling during liver tumor development.
overexpression of INPP4B promotes NPM1-mutated leukemia cell proliferation through SGK3 activation. High levels of INPP4B are at least partially induced by the NPM1 mutant via ERK/Ets-1 signaling.
Hence we concluded that miR1443p which is frequently downregulated in hepatocellular carcinoma (HCC) can inhibit proliferation migration and repress angiogenesis by regulating SGK3 activation with PI3K independent signal pathway and acts as a prognostic factor for HCC patients.
SGK3 a kinase transcriptionally regulated by estrogen receptor alpha (ERalpha) in breast cancer sustains ERalpha signaling and drives the acquired aromatase inhibitors resistance by protecting against endoplasmic reticulum (EnR) stress-induced ERalpha downregulation and cell death through preserving SERCA2b function.
Data show that activation of serum- and glucocorticoid-regulated kinase 3 (SGK3) plays an important role in inositol polyphosphate 4-phosphatase type II (INPP4B)-mediated melanoma cell proliferation.
Breast cancers harboring oncogenic PIK3CA activate SGK3 signaling while suppressing Akt indicative of oncogenic functions for both INPP4B and SGK3 in these tumors.
VPS34-IN1 will provide a useful tool to decipher the kinase-dependent functions of Vps34 with acute changes in SGK3 phosphorylation and subcellular localization being new biomarkers of Vps34 activity
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