Meizhi Wang1, Hui Gao2, Haijun Qu3, Jing Li3, Kaili Liu2, Zhiwu Han4. 1. Department of Critical Care Medicine, The Affiliated Hospital of Qingdao University, Qingdao, China. 2. Department of Pharmacology, School of Pharmacy, Qingdao University, Qingdao, China. 3. Department of Pharmacy, The Affiliated Hospital of Qingdao University, Qingdao, China. 4. Department of Pharmacy, The Affiliated Hospital of Qingdao University, Qingdao, China. Electronic address: drzhiwuhan@163.com.
Abstract
BACKGROUND: The most frequent type of renal cell carcinoma is called clear-cell renal cell carcinoma (ccRCC) which is associated with a poor prognosis. It has been observed that miR-137 is aberrantly expressed in many different kinds of human malignancies including ccRCC. This research aims to examine the role of miR-137 in ccRCC. METHODS: Quantitative RT-PCR (qRT-PCR) was applied to measure miR-137 expression in ccRCC and adjacent noncancerous tissue. Gene expression was determined by western blot. Cell Counting Kit-8 (CCK-8) assay, flow cytometry and Transwell assay were used to determine the effects of miR-137 on cell growth, apoptosis and invasion, respectively. Moreover, xenograft and pulmonary metastasis animal models were established to investigate the role of miR-137 in vivo. RESULTS: Our findings show that there was significant downregulation of miR-137 in ccRCC tissue relative to corresponding non-cancerous tissue. Ectopic miR-137 expression in ccRCC cells led to suppression of cell growth and invasion, as well as apoptosis induction. In contrast, knockdown of miR-137 enhances proliferation and invasion, inhibits apoptosis. It also confirms that miR-137 plays a tumor supressor role in vivo. Mechanically, miR-137 directly targets the 3'-UTR of RLIP76 which is an established oncogene in ccRCC. CONCLUSION: MiR-137 serves as a tumor suppressor, which can be considered a potential therapeutic target in ccRCC.
BACKGROUND: The most frequent type of renal cell carcinoma is called clear-cell renal cell carcinoma (ccRCC) which is associated with a poor prognosis. It has been observed that miR-137 is aberrantly expressed in many different kinds of humanmalignancies including ccRCC. This research aims to examine the role of miR-137 in ccRCC. METHODS: Quantitative RT-PCR (qRT-PCR) was applied to measure miR-137 expression in ccRCC and adjacent noncancerous tissue. Gene expression was determined by western blot. Cell Counting Kit-8 (CCK-8) assay, flow cytometry and Transwell assay were used to determine the effects of miR-137 on cell growth, apoptosis and invasion, respectively. Moreover, xenograft and pulmonary metastasis animal models were established to investigate the role of miR-137 in vivo. RESULTS: Our findings show that there was significant downregulation of miR-137 in ccRCC tissue relative to corresponding non-cancerous tissue. Ectopic miR-137 expression in ccRCC cells led to suppression of cell growth and invasion, as well as apoptosis induction. In contrast, knockdown of miR-137 enhances proliferation and invasion, inhibits apoptosis. It also confirms that miR-137 plays a tumor supressor role in vivo. Mechanically, miR-137 directly targets the 3'-UTR of RLIP76 which is an established oncogene in ccRCC. CONCLUSION:MiR-137 serves as a tumor suppressor, which can be considered a potential therapeutic target in ccRCC.