Li Pan1, Yi Li2, Li Jin1, Jing Li3, Aixiang Xu4. 1. Radiotherapy Department, Sichuan Cancer Hospital & Institute, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China. 2. Department of Gastroenterology and Hepatology, Academy of Medical Sciences and Sichuan Provincial People's Hospital, Affiliated Hospital of University of Electronic Science and Technology of China, Chengdu, 610000, Sichuan, China. 3. Department of General Internal Medicine, Sichuan Cancer Hospital & Institute, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China. Electronic address: ligu637279897@163.com. 4. Department of Outpatient, Zaozhuang Traditional Chinese Medicine Hospital, No. 2666 Taihang Mountain Road, Xuecheng District, Zaozhuang, 277000, Shandong, China. Electronic address: zai47077303962@163.com.
Abstract
BACKGROUND: Colorectal cancer (CRC) ranks the third among all common malignancy worldwide. Long noncoding RNAs (lncRNAs) have been demonstrated as implicated in CRC, but the roles of many lncRNAs in CRC remain unclear. Exploration of lncRNA TRMP2-AS and its nearby gene in CRC progress was the focus of current study. METHODS: The expression of TRPM2-AS and its nearby mRNA TRPM2 was measured by using RT-qPCR. The protein levels of TRPM2 and TAF15 were determined using western blot. Cell proliferation was detected by using CCK-8, colony formation and EdU assays. The interaction between TAF15 and TRPM2-AS or TRPM2 was evaluated by RNA pull-down and RIP assays. The TRPM2 mRNA stability was probed using the transcriptional inhibitor Actinomycin D. RESULTS: TRPM2-AS was significantly upregulated in CRC cells. Knock-down of TRPM2-AS inhibited CRC cell proliferation. Mechanically, TRPM2-AS directly interacted with RNA-binding protein (RBP) TAF15 and thus maintained the mRNA stability of TRPM2. TRPM2 was a prerequisite for TRPM2-AS to exert its promoting function in CRC cell proliferation. CONCLUSION: This research demonstrated that TRPM2-AS facilitated proliferation of CRC cells by enhancing TAF15-mediated mRNA stability of TRPM2, unmasking the role of TRPM2-AS in CRC.
BACKGROUND:Colorectal cancer (CRC) ranks the third among all common malignancy worldwide. Long noncoding RNAs (lncRNAs) have been demonstrated as implicated in CRC, but the roles of many lncRNAs in CRC remain unclear. Exploration of lncRNA TRMP2-AS and its nearby gene in CRC progress was the focus of current study. METHODS: The expression of TRPM2-AS and its nearby mRNA TRPM2 was measured by using RT-qPCR. The protein levels of TRPM2 and TAF15 were determined using western blot. Cell proliferation was detected by using CCK-8, colony formation and EdU assays. The interaction between TAF15 and TRPM2-AS or TRPM2 was evaluated by RNA pull-down and RIP assays. The TRPM2 mRNA stability was probed using the transcriptional inhibitor Actinomycin D. RESULTS:TRPM2-AS was significantly upregulated in CRC cells. Knock-down of TRPM2-AS inhibited CRC cell proliferation. Mechanically, TRPM2-AS directly interacted with RNA-binding protein (RBP) TAF15 and thus maintained the mRNA stability of TRPM2. TRPM2 was a prerequisite for TRPM2-AS to exert its promoting function in CRC cell proliferation. CONCLUSION: This research demonstrated that TRPM2-AS facilitated proliferation of CRC cells by enhancing TAF15-mediated mRNA stability of TRPM2, unmasking the role of TRPM2-AS in CRC.
Authors: José Ricardo Parreira; Lorenzo Enrique Hernández-Castellano; Anastasio Argüello; Juan Capote; Noemí Castro; Susana de Sousa Araújo; André Martinho de Almeida Journal: BMC Genomics Date: 2020-09-14 Impact factor: 3.969