STIL Promotes the Proliferation of Colon Cancer Cells through Regulating CDK1
LIU Jiwei1, SHI Lei2, PENG Jikui3, WANG Yanli3, HUANG Dongqin3, WANG Yongqiang3*
This study aims to study the effect of silencing STIL on the proliferation of colon cancer cells and its molecular mechanism. The present study constructed lentivirus carrying shRNA (short hairpin RNA) against STIL and shCtrl (scrambled shRNA), infected tumor cells with these lentiviruses, and screened STIL stably silenced cells using the puromycin resistance. Then, CCK-8 assay was used to detect cell proliferation, colony formation assay was used to detect clonogenicity, and flow cytometry assay was employed to detect cell cycle distribution and proportion of apoptotic cells in shSTIL- and shCtrl-subgroups. The tumor volume and weight were monitored in nude mice which were subcutaneously injected with stably transfected cells. After STIL was silenced, the proliferation and clonogenicity of colon cancer cells were significantly inhibited, the proportion of apoptotic cells was significantly increased, and the proportion of cells blocked in G2/M phase were significantly increased. Moreover, compared with the shCtrl subgroup, the tumor volume and weight in shSTIL group were significantly retarded. In addition, STIL positively regulated the expression of CDK1, and CDK1 inhibitors could remarkably attenuate the proliferation and clonal formation of STIL overexpressed colon cancer cells. STIL promotes the proliferation of colon cancer cells by regulating the expression of CDK1.
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