Rce1 expression in renal cell carcinoma and its regulatory effect on 786-O cell apoptosis through endoplasmic reticulum stress

Ras and a-factor-converting enzyme 1 （Rcel） is located in the endoplasmic reticulum （ER） and is thought to be responsible for endoproteolytic processing of the vast majority of CAAX proteins. Endoplasmic reticulum stress （ERS） plays an important role in renal cell carcinoma （RCC）; however, the expression and role of Rcel in RCC have not been extensively studied. We aimed to investigate the expression of Rcel in RCC tissues and its molecular mechanism in ERS-induced apoptosis in RCC 786-0 cells. We first used western blotting, quantitative reverse transcriptase- polymerase chain reaction, and immunohistochemistry to detect the Rcel expression in renal carcinoma tissues and paracancerous tissues. It was found that Rcel expression was upregulated in RCC tissues, and its positive expression level was strongly associated with clinicopathologic features. Next, we detected the expression of Rcel in human embryonic kidney cell line HEK293 and human renal carcinoma cell lines 786-0, ACHN, and A498. Higher expression of Rcel was found in human renal carcinoma cell lines, especially in 786-0 cells. Knockdown of Rcel in 786-0 cells increased apoptosis and inhibited proliferation （P 〈 0.05）. Moreover, downregulation of Rcel upregulated the expression of the pro-apoptotic protein Bax, but downregulated the expression of the anti-apoptotic protein Bcl-2. Further studies showed that downregulation of Rcel also affected the expression of ERS factors. In conclusion, our results indicated that Rcel plays a key role in RCC. Low expression of Rcel might indirectly increase apoptosis and inhibit proliferation of renal carcinoma cells through ERS.