@Article{096504015X14452563486057,
AUTHOR = {Zhi-jian Meng, Ke Tao},
TITLE = {Enhancement of Chemosensitivity by Stathmin-1 Silencing in Gastric Cancer Cells In Situ and In Vivo},
JOURNAL = {Oncology Research},
VOLUME = {23},
YEAR = {2015},
NUMBER = {1-2},
PAGES = {35--41},
URL = {http://www.techscience.com/or/v23n1-2/57568},
ISSN = {1555-3906},
ABSTRACT = {Reports show that the stathmin gene may have a close relationship with tumor chemotherapeutic sensitivity. 
However, the effect of stathmin-1 on the chemosensitivity of gastric cancer to docetaxel has not been clearly 
determined. siRNA targeting stathmin-1 was introduced. The cell growth inhibition, expression of associated 
proteins, cell cycle, and apoptosis were evaluated by MTT, Western blot, and flow cytometric assays, respectively. The influence of silencing stathmin-1 was detected in situ and in vivo. SGC7901/docetaxel cells are the 
drug-resistant cells. After silencing stathmin-1, the resistance index (RI) reduced to 3.41, the expressions of 
STMN-1, MDR1, and ERCC1 were downregulated, but caspase 3 was upregulated. Stathmin-1 siRNA could 
improve the chemosensitivity of gastric cancer cells to docetaxel, making the percentage of cells at the sub-G<sub>1</sub>
stage increase and promote apoptosis. The growth of transplantation tumor was significantly suppressed. 
Therefore, stathmin-1 might be a potential target for enhancing the chemosensitivity of gastric cancer.},
DOI = {10.3727/096504015X14452563486057}
}