Yue Zhu1,2, Yujie Gan1, Renrui Zou1, Huanhuan Sha1, Ya Lu1, Yuan Zhang1, Jifeng Feng1. 1. The Affiliated Cancer Hospital of Nanjing Medical University, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research Nanjing 210009, Jiangsu, China. 2. Nanjing Jinling Hospital Nanjing 210002, Jiangsu, China.
Abstract
PURPOSE: Colorectal cancer (CRC) is one of the most frequent tumors and causes of mortality worldwide. Ubiquitin ligase was reported to regulate multiple cellular processes, including tumorigenesis. As ubiquitin E3 ligases, RING-finger proteins play a key role in physiological and pathophysiological processes. METHODS: We compared the expression levels of RNF128 in CRC tissues by western-blotting and qRT-PCR. Knockdown and overexpression of RNF128 were performed to examine its effect on proliferation and metastasis of CRC cells. Using western blot and co-immunoprecipitation assays, we explored the possible mechanisms underlying the effect of RNF128 in CRC cells. RESULTS: We found that the expression level of RNF128 was correlated with the CRC tumorigenicity. Overexpression or knockdown of RNF128 suppressed or elevated CRC cell proliferation, migration and invasion, respectively. We further determined that RNF128 regulated β-catenin ubiquitination and thus inhibited Wnt/β-catenin signaling in CRC cells. CONCLUSION: Our research demonstrated that RNF128 inhibited cell proliferation and metastasis of CRC cells via Wnt/β-catenin signaling-mediated deubiquitination. AJTR
PURPOSE: Colorectal cancer (CRC) is one of the most frequent tumors and causes of mortality worldwide. Ubiquitin ligase was reported to regulate multiple cellular processes, including tumorigenesis. As ubiquitin E3 ligases, RING-finger proteins play a key role in physiological and pathophysiological processes. METHODS: We compared the expression levels of RNF128 in CRC tissues by western-blotting and qRT-PCR. Knockdown and overexpression of RNF128 were performed to examine its effect on proliferation and metastasis of CRC cells. Using western blot and co-immunoprecipitation assays, we explored the possible mechanisms underlying the effect of RNF128 in CRC cells. RESULTS: We found that the expression level of RNF128 was correlated with the CRC tumorigenicity. Overexpression or knockdown of RNF128 suppressed or elevated CRC cell proliferation, migration and invasion, respectively. We further determined that RNF128 regulated β-catenin ubiquitination and thus inhibited Wnt/β-catenin signaling in CRC cells. CONCLUSION: Our research demonstrated that RNF128 inhibited cell proliferation and metastasis of CRC cells via Wnt/β-catenin signaling-mediated deubiquitination. AJTR
Authors: Cara Haymaker; Yi Yang; Junmei Wang; Qiang Zou; Anupama Sahoo; Andrei Alekseev; Divyendu Singh; Krit Ritthipichai; Yared Hailemichael; Oanh N Hoang; Hong Qin; Kimberly S Schluns; Tiejun Wang; Willem W Overwijk; Shao-Cong Sun; Chantale Bernatchez; Larry W Kwak; Sattva S Neelapu; Roza Nurieva Journal: Nat Commun Date: 2017-08-10 Impact factor: 14.919