RUVBL1 accelerates tongue squamous cell carcinoma by mediating CRaf/MEK/ERK pathway

Xin-Yu Zhang; Yang Liu; Qiong Rong; Ming-Yue Qi; Hui Guo

doi:10.1016/j.isci.2024.109434

RUVBL1 accelerates tongue squamous cell carcinoma by mediating CRaf/MEK/ERK pathway

iScience. 2024 Mar 6;27(4):109434. doi: 10.1016/j.isci.2024.109434. eCollection 2024 Apr 19.

Authors

Xin-Yu Zhang¹, Yang Liu², Qiong Rong¹, Ming-Yue Qi², Hui Guo¹

Affiliations

¹ The First People's Hospital of Yunnan Province, Affiliated Hospital of Kunming University of Science and Technology, Kunming, Yunnan Province 650032, China.
² Kunming University of Science and Technology, Kunming, Yunnan Province 650500, China.

Abstract

RAF/MEK/ERK pathway is frequently activated in tumor. Therefore, this study will investigate the function of RUVBL1 (RAF-binding protein) in tongue squamous cell carcinoma (TSCC). Bioinformatics was performed to identify differentially expressed mRNAs (DE-mRNAs) in TCGA-oral squamous cell carcinoma, GSE13601, and GSE34105 datasets. A total of 672 shared DE-mRNAs were identified in three datasets, and they are regulating metastasis and angiogenesis. Patients with RUVBL1 low expression had high overall survival. Overexpressing RUVBL1 enhanced the viability, wound healing percentage, invasion, sphere formation, angiogenesis, and resistance to cisplatin and 5-fluorouracil in CAL-27 and SCC-4 cells, and the opposite results were obtained by knocking down RUVBL1. Moreover, overexpression of RUVBL1 bolstered tumor growth in vivo. Strikingly, RUVBL1 diminished the phosphorylation of CRAF Ser259, which led to activation of the MEK/ERK pathway. In conclusion, RUVBL1 contributes to the malignant biological behavior of TSCC via activating the CRAF/MEK/ERK pathway. This provides molecular mechanisms and perspectives for targeted therapy of the CRAF/MEK/ERK pathway.

Keywords: Cancer; Cell biology; Molecular biology.