Zhao Ping, Guan Hai-Tao, Dai Zhi-Jun, Ma Yu-Guang, Liu Xiao-Xu, Wang Xi-Jing
Department of Gastroenterology, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, P.R. China.
Oncol Res. 2016 Oct 27;24(6):437-445. doi: 10.3727/096504016X14685034103554.
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.
富含半胱氨酸的酸性分泌蛋白/骨连接蛋白、CWCV和Kazal样结构域蛋白聚糖(testican)1(SPOCK1),即睾丸蛋白聚糖-1,被发现与肿瘤的发生发展有关。然而,在结直肠癌(CRC)中,SPOCK1的表达模式及其功能作用仍未得到充分研究。在本研究中,我们探讨了SPOCK1在CRC中的作用。我们的结果表明,SPOCK1在CRC细胞系中过表达。SPOCK1基因沉默显著抑制了体外增殖和体内肿瘤生长。此外,SPOCK1基因沉默通过逆转CRC细胞中的上皮-间质转化(EMT)过程,显著减弱了迁移/侵袭能力。最后,敲低SPOCK1明显降低了HCT116细胞中p-PI3K和p-Akt的蛋白表达水平。总之,我们的研究首次证明,敲低SPOCK1可抑制CRC细胞的增殖和侵袭,可能是通过PI3K/Akt信号通路实现的。因此,SPOCK1可能是治疗CRC的一个潜在治疗靶点。