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Ribosomal protein L22-like1 promotes prostate cancer progression by activating PI3K/Akt/mTOR signalling pathway |
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| Authors: | Xiaoyu Yi Chao Zhang Baojie Liu Guojun Gao Yaqi Tang Yongzheng Lu Zhifang Pan Guohui Wang Weiguo Feng |
| Institution: | 1. School of Life Science and Technology, Weifang Medical University, Weifang, China
Contribution: ?Investigation (equal), Methodology (equal);2. Department of Urology Surgery, Shandong Cancer Hospital and Institute, Jinan, China Department of Urology Surgery, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, China Contribution: Data curation (equal), Formal analysis (equal);3. School of Life Science and Technology, Weifang Medical University, Weifang, China Contribution: Formal analysis (equal);4. Department of Urology Surgery, Affiliated Hospital of Weifang Medical University, Weifang, China Contribution: Formal analysis (equal), Methodology (equal);5. School of Life Science and Technology, Weifang Medical University, Weifang, China Contribution: ?Investigation (equal);6. School of Life Science and Technology, Weifang Medical University, Weifang, China Contribution: Data curation (equal);7. School of Life Science and Technology, Weifang Medical University, Weifang, China |
| Abstract: | Prostate cancer (PCa) is one of the most common malignancies in men. Ribosomal protein L22-like1 (RPL22L1), a component of the ribosomal 60 S subunit, is associated with cancer progression, but the role and potential mechanism of RPL22L1 in PCa remain unclear. The aim of this study was to investigate the role of RPL22L1 in PCa progression and the mechanisms involved. Bioinformatics and immunohistochemistry analysis showed that the expression of RPL22L1 was significantly higher in PCa tissues than in normal prostate tissues. The cell function analysis revealed that RPL22L1 significantly promoted the proliferation, migration and invasion of PCa cells. The data of xenograft tumour assay suggested that the low expression of RPL22L1 inhibited the growth and invasion of PCa cells in vivo. Mechanistically, the results of Western blot proved that RPL22L1 activated PI3K/Akt/mTOR pathway in PCa cells. Additionally, LY294002, an inhibitor of PI3K/Akt pathway, was used to block this pathway. The results showed that LY294002 remarkably abrogated the oncogenic effect of RPL22L1 on PCa cell proliferation and invasion. Taken together, our study demonstrated that RPL22L1 is a key gene in PCa progression and promotes PCa cell proliferation and invasion via PI3K/Akt/mTOR pathway, thus potentially providing a new target for PCa therapy. |
| Keywords: | invasion PI3K/Akt/mTOR proliferation prostate cancer RPL22L1 |