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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 and extracellular signalregulated kinase (ERK) signaling pathways and the expression of RSK4 was altered by DNA methylation 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(RCC)tissues, analysed relationship between RSK4 expression and clinicopathological features of RCC patients and explored potential molecular mechanisms of RSK4 in RCC cell lines; expression pattern and molecular mechanisms of RSK4 in RCCs indicate it could be a potential independent prognostic factor
Overexpression of RSK3 or RSK4 supports tumor cell proliferation upon PI3K inhibition both in vitro and in vivo therby contributing to drug resistance.
findings reveals a major role of PRKX, TTBK2 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.
The expression level of RSK-4 mRNA in breast cancer was significantly lower than those in normal breast tissues and breast benign lesions tissues. The down-regulation of RSK-4 expression in breast caner suggests that it is a breast cancer suppressor gene.
A total of six novel and 11 known single nucleotide polymorphisms were identified. Further studies are warranted to analyze the candidate genes at Xq11.1-q21.33.
Data indicate that RSK4 appears to be epigenetically silenced in endometrial cancer as evidenced by hypermethylation.
importance of RSK4 for regulating senescence and indicate that downregulation of this kinase could be an important element in facilitating cell transformation.
The unusual regulation and growth factor-independent activity of ribosomal S6 kinase 4 (RSK4) indicate that it is functionally distinct from other RSKs and may explain why RSK4 can participate in non-growth factor signaling.
Downregulation of RPS6KA6 is associated with colon carcinoma.
RT-PCR data show high expression of putative tumor suppressor genes Rsk4 and RbAp46 in 47% and 79% of breast carcinoma cases, respectively, whereas Cldn2 was down-regulated in 52% of breast cancer cases compared with normal adjacent tissues.
RSK4 expression may limit the oncogenic, invasive, and metastatic potential of breast cancer cells.
Results support the concept that RSK4 may be an important tumor suppressor gene by modulating senescence induction and contributing to cell proliferation control in colon carcinogenesis and renal cell carcinomas.
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