Yang Yu1, Zhuo Chang2, Chao Han3, Lingling Zhuang4, Chongzhi Zhou3, Xiaosheng Qi3, Zhihai Peng5. 1. Department of General Surgery, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200080, China. Electronic address: shmuyuyang@163.com. 2. Department of Pediatric Endocrinology and Inherited Metabolic Diseases, Children's Hospital of Fudan University, Shanghai, China. 3. Department of General Surgery, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200080, China. 4. Department of Ultrasound, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China. 5. Department of General Surgery, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200080, China. Electronic address: Pengzhihai1958@163.com.
Abstract
BACKGROUND: Increasing evidence has found that the dysregulation of long non-coding RNAs (lncRNAs) may be important indicators in tumorigenesis. MYC-induced long non-coding RNA (MINCR) has been found to be related with some cancers, such as non-small cell lung cancer and gallbladder cancer. Besides, MINCR has potentially prognostic value for colon cancer (CC) patients' prognosis, yet its function and molecular mechanism in CC are not explored. METHODS: qRT-PCR evaluated gene expression, and western blot detected protein level. In vitro and in vivo experiments were adopted to understand the biological role of MINCR in CC. TOP/FOP Flash assay was performed to measure the activity of Wnt/β-catenin pathway. RNA pull down, luciferase reporter and RIP assays were utilized to analyze the relationship among genes. Immunohistochemistry and HE staining techniques were utilized to evaluate Ki67 staining in xenografts. RESULTS: MINCR was up-regulated in CC cells. Knockdown of MINCR suppressed cell proliferation and migration. MINCR could up-regulate CTNNB1 via sequestering miR-708-5p, resulting in activated Wnt/β-catenin pathway. The addition of LiCl treatment, miR-708-5p inhibitor or pcDNA3.1/CTNNB1 abolished the inhibitory impacts induced by MINCR silence in CC progression. CONCLUSION: MINCR sponges miR-708-5p to up-regulate CTNNB1 and activate Wnt/β-catenin pathway, thus promoting the development CC. Targeting MINCR might shed new light on the therapeutic strategies of CC.
BACKGROUND: Increasing evidence has found that the dysregulation of long non-coding RNAs (lncRNAs) may be important indicators in tumorigenesis. MYC-induced long non-coding RNA (MINCR) has been found to be related with some cancers, such as non-small cell lung cancer and gallbladder cancer. Besides, MINCR has potentially prognostic value for colon cancer (CC) patients' prognosis, yet its function and molecular mechanism in CC are not explored. METHODS: qRT-PCR evaluated gene expression, and western blot detected protein level. In vitro and in vivo experiments were adopted to understand the biological role of MINCR in CC. TOP/FOP Flash assay was performed to measure the activity of Wnt/β-catenin pathway. RNA pull down, luciferase reporter and RIP assays were utilized to analyze the relationship among genes. Immunohistochemistry and HE staining techniques were utilized to evaluate Ki67 staining in xenografts. RESULTS:MINCR was up-regulated in CC cells. Knockdown of MINCR suppressed cell proliferation and migration. MINCR could up-regulate CTNNB1 via sequestering miR-708-5p, resulting in activated Wnt/β-catenin pathway. The addition of LiCl treatment, miR-708-5p inhibitor or pcDNA3.1/CTNNB1 abolished the inhibitory impacts induced by MINCR silence in CC progression. CONCLUSION:MINCR sponges miR-708-5p to up-regulate CTNNB1 and activate Wnt/β-catenin pathway, thus promoting the development CC. Targeting MINCR might shed new light on the therapeutic strategies of CC.
Authors: Chien-Wei Lee; Yi-Fan Chen; Allen Wei-Ting Hsiao; Amanda Yu-Fan Wang; Oscar Yuan-Jie Shen; Belle Yu-Hsuan Wang; Lok Wai Cola Ho; Wei-Ting Lin; Chung Hang Jonathan Choi; Oscar Kuang-Sheng Lee Journal: J Adv Res Date: 2021-11-19 Impact factor: 12.822
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