MCOLN2 plays an oncogenic role in prostate cancer progression
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摘要Prostate cancer originated from the glandular epithelial cells is one of the most common malignancies and the second leading cause of cancer-related death in males worldwide. However, the molecular mechanism of prostate cancer progression remains obscure. MCOLN2 is Ca2+-permeable cationic channel that belongs to the transient receptor potential (TRP) protein superfamily. This protein shares a conserved structure of six transmembrane helices with differing cytoplasmic oriented N- and C-terminal domains. Previous studies suggest that MCOLN2 may play a role in the immune system by activating chemokines CCL2. However, there is still no report about the role of MCOLN2 during prostate cancer development.

By bioinformatic analysis, we found that mcoln2 is overexpressed in prostate cancer tissues compared with adjacent normal tissues. The patients with higher MCOLN2 expression tend to have poor overall survival rates. Western blot and qRT-PCR analysis showed that MCOLN2 expression was upregulated in prostate cancer cell lines PC3 and Du145 when compared with benign prostate epithelial cell line BPH. Knockdown of endogenous MCOLN2 expression in PC3 and Du145 cells inhibited cell growth and foci formation by CCK-8 assay and crystal violet staining, respectively. Furthermore, silencing of MCOLN2 in PC3 and Du145 cells inhibited cell migration and invasion in transwell assay. Taken together, our results suggest an oncogenic role of MCOLN2 in prostate cancer progression.
著者Hongyan YU, Xiaoqiang YAO
會議名稱The 12th International Symposium on Calcium Signaling in China (SCSC)
會議地點Shenyang, Liaoning Province

上次更新時間 2018-10-10 於 17:07