Abstract
In clinic, we examined the expression of protein kinase C (PKC)-α and Dicer in the samples of bladder cancer patients, and found that the two proteins have a line correlation. Our study confirmed this correlation existing by clearing the decreasing expression of Dicer after the PKC-α knockdown. Treatment of bladder cancer cell lines (T24, 5637) with the PKC-α or Dicer knockdown and the PKC inhibitors (Calphostin C and Gö 6976) can promote the apoptosis. Inhibition of PKC can increase the activities of caspase-3 and PARP, however, decrease the expression of Dicer. And knockdown of the PKC-α or Dicer can also activate the caspase-3 or the PARP. Considering the reduction of PKC-α can induce the Dicer down-regulation, we make the conclusion that the reduction of PKC-α can promote the apoptosis via the down-regulation of Dicer in bladder cancer.
Highlights
Bladder cancer (BC) is one of the most recurrent malignant tumours and the second most common urologic cancer [1]
Real-time PCR results of Dicer and protein kinase C (PKC)-a expression in clinical BC samples showed that the both proteins were produced more in the high-grade papillary urothelial carcinoma (HGPUC) than in the lowgrade papillary urothelial carcinoma (LGPUC; Dicer:
We found that the two BC cell lines with PKC-a and Dicer knockdown were more sensitive to the apoptosis than those with mock knockdown after 24 hrs cultured respectively (Fig. 2, phase Q4)
Summary
Bladder cancer (BC) is one of the most recurrent malignant tumours and the second most common urologic cancer [1]. As the central hub of many signal transduction process, protein kinase C (PKCs) are involved in various cellular processes such as regulation of gene expression, proliferation, cell junctions, apoptosis, and migration. Many agents and factors can modulate the apoptosis of carcinoma cells via protection or inhibition of the PKC-a [3]. Because of the only copy of Dicer in the human being’s genome, inhibiting or knockdown of it should theoretically produce cells that are deficient in miRNAs. Array expression profiling analysis has revealed a global reduction of miRNAs expression in various cancer models. Array expression profiling analysis has revealed a global reduction of miRNAs expression in various cancer models This observation led to a hypothesis that the low expression of Dicer could be the key factor in tumour tissue initiation or program death. Our results point to another pathway of PKC-a regulation of apoptosis and suggest that Dicer can be involved in this process
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