医学分子生物学杂志 ›› 2025, Vol. 22 ›› Issue (5): 494-499.doi: 10.3870/j.issn.1672-8009.2025.05.012

• 论著 • 上一篇    下一篇

STAT3 调控 Wnt / β-catenin 信号通路对结直肠癌干细胞增殖和自噬的机制研究 #br#

  

  1. 邯郸市中心医院药学部 河北省邯郸市, 056001
  • 出版日期:2025-09-30 发布日期:2025-10-09
  • 基金资助:
    邯郸市科学技术研究与发展计划项目 (No. 23422083002ZC)

Effect of STAT3 on Proliferation and Autophagy of Colorectal Cancer Stem Cells by Wnt / β-catenin Signaling Pathway #br#

  1. Department of Pharmacy, Handan Central Hospital, Handan, Hebei, 056001, China
  • Online:2025-09-30 Published:2025-10-09

摘要: 目的 分析信号转导子和激活子 3 (signal transducer and activator of transcription 3, STAT3) 通过调控 β-catenin 信号通路对结直肠癌干细胞增殖和自噬的影响方法 结直肠癌细胞经培养分选后获得结直肠癌干细胞, 分为 CCSC 、 STAT3 、 STAT3 ihibitor 、 STAT3 inhibitor + Wnt / β-catenin-inhibitor 检测各组细胞增殖率凋亡率增殖凋亡自噬相关蛋白、 Wnt / β-catenin 信号通路蛋白表达结果 癌组织 CD133 + CD44 + 细胞 STAT3 的表达量高于癌旁组织 CD133 - CD44 - 细胞 ( P< 0. 05)。 CCSC 组比较, STAT3 STAT3、 CyclinD1、 Bcl-2、 P62、 Wnt2、 β-catenin 的表达水平增殖率升高, 凋亡率、 Caspase-3、Bax、 Beclin1 的表达水平降低; CCSC 、 STAT3 组比较, STAT3 ihibitor 、 STAT3 inhibitor + Wnt / β- catenin-inhibitor STAT3、 CyclinD1、 Bcl-2、 P62、 Wnt2、 β-catenin 的表达水平增殖率降低, 凋亡率、Caspase-3、 Bax、 Beclin1 的表达水平升高 ( P< 0. 05); STAT3 ihibitor 组比较, STAT3 inhibitor + Wnt / β- catenin-inhibitor STAT3、 CyclinD1、 Bcl-2、 P62、 Wnt2、 β-catenin 表 达 水 平增 殖 率 降 低, 凋 亡 率、caspase-3、 Bax、 Beclin1 的表达水平升高 (P< 0. 05)。 结论 结直肠癌干细胞经下调 STAT3 干预后增殖率下降, 凋亡率上升, 自噬增强, 其机制可能与 Wnt / β-catenin 信号通路被抑制有关

关键词:

信号转导子和激活子 3, Wnt / β-连环蛋白, 结直肠癌, 干细胞, 增殖, 自噬

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.

Key words:

signal transducer and activator of transcription 3, Wnt / β-catenin, colorectalcancer, stem cell, proliferation, autophagy

中图分类号: