Int J Biol Sci 2022; 18(1):124-139. doi:10.7150/ijbs.63598 This issue

Research Paper

RNA-binding motif protein 10 represses tumor progression through the Wnt/β- catenin pathway in lung adenocarcinoma

Yingyue Cao1, Jianxiong Geng1, Xin Wang1, Qingwei Meng1, Shanqi Xu1, Yaoguo Lang1, Yongxu Zhou2, Lishuang Qi3, Zijie Wang1, Zixin Wei1, Yan Yu1✉, Shi Jin4✉, Bo Pan1✉

1. Department of Medical Oncology, Harbin Medical University Cancer Hospital, Haping Road No 150, Harbin 150040, China.
2. Department of hepatopancreatobiliary surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, 150040, China.
3. College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150040, China.
4. National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital & Shenzhen Hospital, Chinese Academy of Medical Sciences and Perking Union Medical College, Shenzhen, 518116, China.

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Citation:
Cao Y, Geng J, Wang X, Meng Q, Xu S, Lang Y, Zhou Y, Qi L, Wang Z, Wei Z, Yu Y, Jin S, Pan B. RNA-binding motif protein 10 represses tumor progression through the Wnt/β- catenin pathway in lung adenocarcinoma. Int J Biol Sci 2022; 18(1):124-139. doi:10.7150/ijbs.63598. Available from https://www.ijbs.com/v18p0124.htm

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Abstract

Graphic abstract

RNA-binding motif protein 10 (RBM10), one of the members of the RNA-binding protein (RBP) family, has a tumor suppressor role in multiple cancers. However, the functional role of RBM10 in lung adenocarcinoma (LUAD) and the underlying molecular mechanism remains unclear. In this study, we observed that RBM10 is significantly downregulated in LUAD tissues compared with normal tissues. Low RBM10 expression is significantly associated with poor outcome of LUAD patients. In vitro and in vivo experiments show that RBM10 inhibits cell proliferation, metastasis and EMT progression in LUAD. Mechanistically, we demonstrate that RBM10 interacts with β-catenin interacting protein 1 (CTNNBIP1) and positively regulates its expression, disrupting the binding of β-catenin to the transcription factor TCF/LEF, thereby inactivating the Wnt/β-catenin pathway. In conclusion, this is the first study reporting the role of RBM10 in suppressing LUAD progression at least via partly inactivating the Wnt/β-catenin pathway, which provides new insights into the tumorigenesis and metastasis of LUAD. Thus, RBM10 may be a promising new therapeutic target or clinical biomarker for LUAD therapy in the future.

Keywords: RBM10, progression, Wnt/β-catenin pathway, CTNNBIP1, lung adenocarcinoma