LASP-1 induces proliferation, metastasis and cell cycle arrest at the G2/M phase in gallbladder cancer by down-regulating S100P via the PI3K/AKT pathway. Issue 2 (28th March 2016)

• Record Type: Journal Article
• Authors: Li, ZhiZhen; Chen, YuanYuan; Wang, XuAn; Zhang, HongChen; Zhang, Yijian; Gao, YaoHui; Weng, Mingzhe; Wang, Lei; Liang, HaiBin; Li, MaoLan; Zhang, Fei; Zhao, Shuai; Liu, Shibo; Cao, Yang; Shu, Yijun; Bao, Runfa; Zhou, Jian; Liu, Xiyong; Yan, Yun; Zhen, Lei; Dong, Qian; Liu, Yingbin
• Is Part Of: Cancer letters. Volume 372:Issue 2(2016)
• Page Start: 239
• Page End: 250
• Publication Date: 2016-03-28
• Subjects: Gallbladder cancer -- LASP-1 -- S100P -- Proliferation -- Metastasis -- Cell cycle; Cancer -- Periodicals; Neoplasms -- Periodicals; Cancer -- Périodiques; Electronic journals; 616.994
• DOI: 10.1016/j.canlet.2016.01.008
• Languages: English
• ISSNs: 0304-3835

Abstract

Highlights: This study investigated the effects of LASP1 and S100P on the growth of GBC cells. LASP-1 effects biological functions of GBC cells by down-regulating S100P via the PI3K/AKT pathway. Abstract: LASP-1 is an actin-binding protein that regulates cytoskeletal dynamics and cell migration. LASP-1 was previously identified in a cDNA library from metastatic breast cancer samples. This protein has since been detected in multiple human cancers, including liver cancer, gastric cancer and pancreatic cancer. S100P is a small calcium-binding protein in the S100 protein family that regulates cellular, physiological and pathological processes in various cancers. However, the clinical significance of LASP-1 and S100P expression in gallbladder cancer (GBC) is not yet clear. In our study, we focused on the clinical significance, biological function and mechanism of LASP-1 in gallbladder cancer and detected LASP-1 and S100P overexpression in GBC tissues. The expression of LASP-1 was significantly correlated with poor prognosis in GBC patients ( P < 0.05). Furthermore, down-regulation of LASP-1 expression resulted in the obvious inhibition of proliferation and migration and caused cell cycle arrest by down-regulating S100P via the PI3K/AKT pathway; in mice, tumor volume was significantly decreased. In conclusion, LASP-1 may act as an oncogene to regulate the expression of S100P to influence cellular functions in GBC. LASP-1 could serve as a genetic treatment target in GBC patients.