Lentivirus-mediated shRNA targeting MUTYH inhibits malignant phenotypes of bladder cancer SW780 cells
Received 15 May 2018
Accepted for publication 23 July 2018
Published 21 September 2018 Volume 2018:11 Pages 6101—6109
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Andrew Yee
Peer reviewer comments 3
Editor who approved publication: Dr Sanjeev Srivastava
Qunjun Gao,1–3 Yuhan Liu,2,3 Haibiao Xie,2,3 Yucheng Zhong,2,3 Xinhui Liao,3 Hengji Zhan,2,3 Qun Zhou,2,3 Mengting Ding,2,3 Kang Yang,2,3 Aolin Li,2,3 Yuchen Liu,2,3 Hongbing Mei,3 Zhiming Cai1–3
1Key Laboratory of Medical Reprogramming Technology, Shenzhen Second People’s Hospital, Guangzhou Medical University, Guangzhou 511436, China; 2Key Laboratory of Medical Reprogramming Technology, Shenzhen Second People’s Hospital, First Affiliated Hospital of Shenzhen University, Shenzhen 518039, China; 3Department of Urology, Shenzhen Second People’s Hospital, First Affiliated Hospital of Shenzhen University, Shenzhen 518039, China
Objectives: MUTYH is a protein-coding gene that takes part in base excision repair. Many previous studies have reported that MUTYH is directly related to hereditary adenomatous polyposis and colorectal cancer and is also associated with other cancers. However, the relationship between MUTYH and bladder cancer (BC) is unknown.
Materials and methods: The expression of MUTYH and clinical characteristics of BC were collected from databases including The Cancer Genome Atlas and Cancer Cell Line Encyclopedia. RNA sequencing and quantitative real-time PCR were used to detect MUTYH expression in SW780 BC cells. The level of MUTYH was stably downregulated by lentivirus-mediated vector in SW780 cells. Cell proliferation was evaluated using Cell Counting Kit-8 assay and 5-ethynyl-20-deoxyuridine assay, migration was detected using scratch assay and Transwell assay, and apoptosis was determined using ELISA.
Results: MUTYH was upregulated in BC tissues and SW780 cells and its expression level was positively associated with the stage and grade of carcinomas. MUTYH was successfully downregulated in SW780 cells by transducing with a lentivirus-mediated shRNA targeting MUTYH. MUTYH knockdown inhibited the proliferation and migration and induced apoptosis in SW780 cells.
Conclusion: Our data suggest that MUTYH is a new participant in bladder urothelial carcinoma. MUTYH may play a role as a biomarker and therapeutic target in BC.
Keywords: MUTYH, bladder cancer, cell proliferation, migration, apoptosis
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