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RSK4 constitutes a putative tumor suppressor gene for non-small cell lung carcinoma.
The regulatory role of RSK4 in breast cancer development was mediated by AKT (Montrer AKT1 Protéines) and extracellular signalregulated kinase (ERK (Montrer EPHB2 Protéines)) signaling pathways and the expression of RSK4 was altered by DNA methylation (Montrer HELLS Protéines) in promoter regions.
RSK4 is expressed at low levels in malignant ovarian tumors, which correlates with advanced stages of the disease.
downregulation of RSK4 expression is indicated to be associated with tumor cell proliferation and invasion, and silencing of the RSK4 may be involved in the development and progression of breast cancer
Low RSK4 expression is correlated with advanced clinical pathologic classifications and is a poor overall survival in colorectal cancer patients
RSK4 mRNA is significantly decreased in most of breast cancer tissues compared with paired non-cancerous tissues, due to promoter hypermethylation; frequent epigenetic inactivation might have a role in precancerous lesions or early cancer
evaluated expression of RSK4 in renal cell carcinoma (Montrer MOK Protéines)(RCC (Montrer XRCC1 Protéines))tissues, analysed relationship between RSK4 expression and clinicopathological features of RCC (Montrer XRCC1 Protéines) patients and explored potential molecular mechanisms of RSK4 in RCC (Montrer XRCC1 Protéines) cell lines; expression pattern and molecular mechanisms of RSK4 in RCCs indicate it could be a potential independent prognostic factor
Overexpression of RSK3 (Montrer RPS6KA2 Protéines) or RSK4 supports tumor cell proliferation upon PI3K (Montrer PIK3CA Protéines) inhibition both in vitro and in vivo therby contributing to drug resistance.
findings reveals a major role of PRKX (Montrer PRKX Protéines), TTBK2 (Montrer TTBK2 Protéines) and RSK4 in triggering Sunitinib resistance formation; data suggest transcriptional regulation of these kinases together with other proteins might play an important role in formation of Sunitinib resistance by affecting transcription factors
Suggest that RSK4 may serve as a mediator of endothelial progenitor cell senescence in diabetes mellitus.
TRAF4 (Montrer TRAF4 Protéines) knockdown significantly inhibited proliferation, invasion and metastasis in the xenograft nude mouse model, possibly involving in the interaction with RSK4.
Rsk4 inhibits the transcriptional activation of specific targets of receptor tyrosine kinase (Montrer ERBB3 Protéines) signaling as well as the activation of ERK (Montrer EPHB2 Protéines)
This gene encodes a member of ribosomal S6 kinase family, serine-threonine protein kinases which are regulated by growth factors. The encoded protein may be distinct from other members of this family, however, as studies suggest it is not growth factor dependent and may not participate in the same signaling pathways.
90 kDa ribosomal protein S6 kinase 6
, S6K-alpha 6
, p90-RSK 6
, ribosomal S6 kinase 4
, ribosomal protein S6 kinase alpha-6
, ribosomal protein S6 kinase polypeptide 6