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Abstract: Objective To investigate the effect of signal transducer and activator of transcription 3 (STAT3) on the proliferation and autophagy of colorectal cancer stem cells. Methods The colorectal cancer stem cells were sorted out from colorectal cancer cells, and were categorized into 4groups: CCSC, STAT3, STAT3 ihibitor, and STAT3 inhibitor + Wnt / β-catenin-inhibitor. The proliferation rate, apoptosis rate, and the expression levels of proteins related to cell proliferation, apoptosis, and autophagy, as well as Wnt / β-catenin signaling pathway proteins, were measured ineach group. Results The expression levels of STAT3 in cancer tissues and CD133 + CD44 + cellswere significantly higher than those in the adjacent tissues and CD133 - CD44 - cells ( P < 0. 05). Compared to the CCSC group, the STAT3 group showed increased expression levels of STAT3, CyclinD1, Bcl-2, P62, Wnt2, and β-catenin, as well as higher proliferation rates, while the apoptosis rate and the expression levels of Caspase-3, Bax, and Beclin1 were reduced. Compared to both the CCSC and STAT3 groups, the STAT3 ihibitor group and the STAT3 inhibitor + Wnt / β- catenin-inhibitor group showed decreased expression levels of STAT3, CyclinD1, Bcl-2, P62, Wnt2, and β-catenin, as well as lower proliferation rates, while the apoptosis rate and the expression of Caspase-3, Bax, and Beclin1 were increased (P < 0. 05). Compared to the STAT3 ihibitorgroup, the STAT3 inhibitor + Wnt / β-catenin-inhibitor group showed decreased expression levels of STAT3, CyclinD1, Bcl-2, P62, Wnt2, and β-catenin, as well as lower proliferation rates, while the apoptosis rate and the expression levels of Caspase-3, Bax, and Beclin1 were increased(P< 0. 05). Conclusion Downregulation of STAT3 inhibits the proliferation, and enhances the apoptosis and autophagy of colorectal cancer stem cells. The mechanism may be related to the inhibition of the Wnt / β-catenin signaling pathway.

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