UPR signaling factors were co-activated and activation of UPR signaling was implicated to the malignant progression and worse prognosis of PCa. The mechanism and function of UPR signaling in PCa are still to be determined. Prostate 77:274-281, 2017. © 2016 Wiley Periodicals, Inc.

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Ras and a-factor-converting enzyme 1 (Rce1) 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 Rce1 in RCC have not been extensively studied. We aimed to investigate the expression of Rce1 in RCC tissues and its molecular mechanism in ERS-induced apoptosis in RCC 786-O cells. We first used western blotting, quantitative reverse transcriptase-polymerase chain reaction, and immunohistochemistry to detect the Rce1 expression in renal carcinoma tissues and paracancerous tissues. It was found that Rce1 expression was upregulated in RCC tissues, and its positive expression level was strongly associated with clinicopathologic features. Next, we detected the expression of Rce1 in human embryonic kidney cell line HEK293 and human renal carcinoma cell lines 786-O, ACHN, and A498. Higher expression of Rce1 was found in human renal carcinoma cell lines, especially in 786-O cells. Knockdown of Rce1 in 786-O cells increased apoptosis and inhibited proliferation (P < 0.05). Moreover, downregulation of Rce1 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 Rce1 also affected the expression of ERS factors. In conclusion, our results indicated that Rce1 plays a key role in RCC. Low expression of Rce1 might indirectly increase apoptosis and inhibit proliferation of renal carcinoma cells through ERS.

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Asparagine-linked glycosylation 13 (ALG13) is a highly conserved protein in most eukaryotes, which belongs to the OTU family. It plays a role in neuroblastoma and non-small cell lung cancer. However, the role of ALG13 in prostate cancer (Pca) and its correlation with tumor-infiltrating immune cells remain unclear. Thus, in this study, we extracted and analyzed The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), Tumor Immune Estimation Resource (TIMER), and Human Protein Atlas (HPA) data sets to study the potential carcinogenic mechanism of ALG13, including ALG13 expression, prognosis and the correlation of ALG13 expression in immune cell infiltration in Pca. Furthermore, the potential biological signaling pathway of ALG13 in Pca was studied by using Gene set enrichment analysis (GSEA). Upstream microRNA and lncRNA related to ALG13 were found through the prediction of miRWalk and starBase. Results showed that ALG13 was highly expressed in Pca tissues and associated with poor overall survival (OS) and disease-specific survival (DSS). ALG13 expression was correlated with immune cell infiltration. In addition, ALG13 was co-expressed with most immune-related genes, and the high-expression of ALG13 was effective for immune-checkpoint blockade treatment. ALG13 may regulate the pathogenesis of Pca through tumor and immune-related pathways. Finally, AL390728.6/hsa-miR-381-3p axis is considered as a potential upstream ncRNA-related pathway of ALG13 in Pca. Our results demonstrate that the ncRNA-mediated upregulation of ALG13 is associated with poor OS in Prostate adenocarcinoma (PRAD) and tumor immune infiltration. ALG13 may be a new potential prognostic biomarker.