@Article{096504016X14685034103554,
AUTHOR = {Ping Zhao, Hai-Tao Guan, Zhi-Jun Dai, Yu-Guang Ma, Xiao-Xu Liu, Xi-Jing Wang},
TITLE = {Knockdown of SPOCK1 Inhibits the Proliferation and Invasion in  Colorectal Cancer Cells by Suppressing the PI3K/Akt Pathway},
JOURNAL = {Oncology Research},
VOLUME = {24},
YEAR = {2016},
NUMBER = {6},
PAGES = {437--445},
URL = {http://www.techscience.com/or/v24n6/57001},
ISSN = {1555-3906},
ABSTRACT = {Sparc/osteonectin, cwcv, and kazal-like domains proteoglycan (testican) 1 (SPOCK1), known as testican-1, 
were found to be involved in the development and progression of tumors. However, in colorectal cancer (CRC), 
the expression pattern of SPOCK1 and its functional role remain poorly investigated. In the present study, 
we explored the role of SPOCK1 in CRC. Our results demonstrated that SPOCK1 is overexpressed in CRC 
cell lines. SPOCK1 silencing significantly inhibited the proliferation in vitro and the tumor growth in vivo. 
Furthermore, SPOCK1 silencing significantly attenuated the migration/invasion by reversing the EMT process 
in CRC cells. Finally, knockdown of SPOCK1 obviously decreased the protein expression levels of p-PI3K and 
p-Akt in HCT116 cells. In total, our study demonstrated for the first time that knockdown of SPOCK1 inhibits the 
proliferation and invasion in CRC cells, possibly through the PI3K/Akt signaling pathway. Therefore, SPOCK1 
may be a potential therapeutic target for the treatment of CRC.},
DOI = {10.3727/096504016X14685034103554}
}