Abstract
BackgroundCDK11p58 is one of the large families of p34cdc2-related kinases whose functions are linked with cell cycle progression, tumorigenesis and apoptotic signaling. Our previous investigation demonstrated that CDK11p58 repressed androgen receptor (AR) transcriptional activity and was involved in the negative regulation of AR function.MethodsCDK11p58 expression was examined in the prostate cancer tissues and adjacent tissues by IHC and qRT-PCR. Cell apoptosis was detected by flow cytometry. The metastasis of cancer cells was evaluated by the Transwell Assay. Finally we further investigated the underlying molecular mechanisms by examining expression levels of relevant proteins using western blot analysis.ResultsWe found that both RNA and protein expression of CDK11p58 were low in prostate cancer tissues compared with its adjacent noncancerous tissues. CDK11p58 promoted the prostate cancer cell apoptosis and inhibited its metastasis in a kinase dependent way. And finally CDK11p58 could inhibit the metastasis of AR positive prostate cancer cells through inhibition of integrin β3 and MMP2.ConclusionsThese data indicate that CDK11p58 is an anti-metastasis gene product in prostate cancer.
Highlights
CDK11, which is encoded by two highly homologous p34cdc2-related genes, Cdc2L1 and Cdc2L2 [1,2], and is known as PITSLRE protein kinase due to the conservedPITSLRE motif within the protein kinase domain [3]
Expression of CDK11 in normal prostate tissues and prostate cancer tissues CDK11p58 is located on human chromosome 1p36.33, a region frequently mutated in various cancers
To investigate the potential role of CDK11p58 in prostate carcinogenesis, we examined the expression of CDK11p58 protein in prostate cancer tissues and adjacent non-cancerous tissues
Summary
CDK11, which is encoded by two highly homologous p34cdc2-related genes, Cdc2L1 and Cdc2L2 [1,2], and is known as PITSLRE protein kinase due to the conservedPITSLRE motif within the protein kinase domain [3]. CDK11p58 is one isoform of CDK11 and is closely related to cell cycle arrest and apoptosis in a kinase-dependent manner [2,4]. Our previous investigation demonstrated that CDK11p58 repressed androgen receptor (AR) transcriptional activity and was involved in the negative regulation of AR function. Methods: CDK11p58 expression was examined in the prostate cancer tissues and adjacent tissues by IHC and qRT-PCR. Results: We found that both RNA and protein expression of CDK11p58 were low in prostate cancer tissues compared with its adjacent noncancerous tissues. CDK11p58 promoted the prostate cancer cell apoptosis and inhibited its metastasis in a kinase dependent way. CDK11p58 could inhibit the metastasis of AR positive prostate cancer cells through inhibition of integrin β3 and MMP2. Conclusions: These data indicate that CDK11p58 is an anti-metastasis gene product in prostate cancer
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