Journal
CANCER LETTERS
Volume 372, Issue 2, Pages 239-250Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2016.01.008
Keywords
Gallbladder cancer; LASP-1; S100P; Proliferation; Metastasis; Cell cycle
Categories
Funding
- National Natural Science Foundation of China [81172026, 81272402, 81301816, 81172029, 91440203, 81402403]
- National High Technology Research and Development Program (863 Program) [2012AA022606]
- Foundation for Interdisciplinary Research of Shanghai Jiao Tong University [YG2011ZD07]
- Shanghai Science and Technology Commission Intergovernmental International Cooperation Project [12410705900]
- Shanghai Science and Technology Commission Medical Guiding Project [12401905800]
- Program for Changjiang Scholars
- Natural Science Research Foundation of Shanghai Jiao Tong University School of Medicine [13XJ10037]
- Leading Talent program of Shanghai and Specialized Research Foundation [20130073130014]
- Interdisciplinary Program of Shanghai Jiao Tong University [14JCRY05]
- Shanghai Rising-Star Program [15QA1403100]
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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 5100 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 signifidantly 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. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
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