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Biochem Biophys Res Commun. 2018 Apr 15;498(4):932-939. doi: 10.1016/j.bbrc.2018.03.084. Epub 2018 Mar 15.

RUVBL1, a novel C-RAF-binding protein, activates the RAF/MEK/ERK pathway to promote lung cancer tumorigenesis.

Author information

1
Faculty of Life Science and Technology, Kunming University of Science and Technology, Kunming, Yunnan, 650500, China; The First People's Hospital of Yunnan Province, Kunming, Yunnan, China.
2
Faculty of Life Science and Technology, Kunming University of Science and Technology, Kunming, Yunnan, 650500, China.
3
The First People's Hospital of Yunnan Province, Kunming, Yunnan, China.
4
Faculty of Life Science and Technology, Kunming University of Science and Technology, Kunming, Yunnan, 650500, China. Electronic address: aslxj@mail.ustc.edu.cn.
5
Faculty of Life Science and Technology, Kunming University of Science and Technology, Kunming, Yunnan, 650500, China. Electronic address: tianruixu@kmust.edu.cn.

Abstract

Lung cancer remains the leading cause of cancer-related deaths in the world. The RAF/MEK/ERK pathway controls many fundamental cellular functions and plays key roles in lung carcinogenesis. However, the proteins that regulate this pathway remain largely unknown. Here, we identified a novel C-RAF-binding protein, RUVBL1, which activates the RAF/MEK/ERK pathway by inhibiting phosphorylation of the C-RAF protein at serine 259. RUVBL1 expression was elevated in lung adenocarcinoma tissues. In addition, knocking out RUVBL1 effectively inhibited the proliferation and invasion of A549 cells. In vivo experiments, RUVBL1 deficiency significantly decreased the tumorigensis of lung cancer. In conclusion, we have shown that RUVBL1 could activate the RAF/MEK/ERK pathway by inhibiting phosphorylation of the C-RAF protein at serine 259, to promote lung cancer progression. Therefore, RUVBL1 could represent a novel therapeutic target for lung cancer treatment.

KEYWORDS:

A549 cells; C-RAF kinase; Lung cancer; RUVBL1

PMID:
29545175
DOI:
10.1016/j.bbrc.2018.03.084
[Indexed for MEDLINE]

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