Premium
LATS 2 induced by TNF ‐alpha and inhibited cell proliferation and invasion by phosphorylating YAP in oral squamous cell carcinoma
Author(s) -
Dong Cong,
Wei KuiJie,
Zhang WenBin,
Sun Hao,
Pan HongYa,
Zhang Lei
Publication year - 2015
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/jop.12317
Subject(s) - cell growth , hippo signaling pathway , cancer research , carcinogenesis , phosphorylation , cell cycle , biology , cell , in vivo , microbiology and biotechnology , cancer , biochemistry , genetics
Objective Many reports indicated LATS2 was a component of the Hippo pathway, could phosphorylate and inactivate YAP, acted as a tumor suppressor in human cancers. But few studies investigated the role of LATS2 in oral squamous cell carcinoma (OSCC) and clarified the mechanisms of regulation of LATS2 expression. Design The expressions of LATS2 and phosphorylated YAP were detected by Western blotting in HN6 cells treated with TNF‐α in different time and different dose. Luciferase reporter assays were performed to detect whether YAP can be phosphorylated by LATS2 in HN6 cells. Cell proliferation, anchorage independent growth in soft agar, transwell cell invasion assay, and nu mice in vivo xenografts growth were performed to study the effects of overexpression of LATS2 on OSCC cells. Results In this study, we confirmed that YAP can be phosphorylated by LATS2. LATS2 can be dose‐ and time‐dependently induced by TNF‐α in HN6 cells. Overexpression of LATS2 inhibited cell proliferation, colony formation, cell invasion, and in vivo xenografts growth in OSCC cells. Conclusion LATS2 could be induced by TNF‐alpha and inhibited cell proliferation and invasion by phosphorylating YAP in OSCC cells. LATS2 might play a role in the tumorigenesis of OSCC and might be a potential therapeutic target in OSCC treatment.