医学分子生物学杂志 ›› 2025, Vol. 22 ›› Issue (5): 488-493.doi: 10.3870/j.issn.1672-8009.2025.05.011

• 论著 • 上一篇    下一篇

脂联素对子宫内膜癌细胞增殖侵袭及 PI3K / AKT / NF-κB通路的影响 #br#

  

  1. 1邯郸市妇幼保健院检验一科 河北省邯郸市, 056001 2邯郸市中心医院妇二科 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:
    河北省医学科学研究课题 (No. 20241717)

Effect of Adiponectin on Endometrial Cancer Cell Growth, Invasion, and PI3K / AKT / NF-κB Pathway #br#

  1. 1Department of Laboratory Medicine, Maternity and Child Health Hospital, Handan, Hebei, 056001, China 2Department of Obstetrics and Gynecology, Handan Central Hospital, Handan, Hebei, 056001, China
  • Online:2025-09-30 Published:2025-10-09

摘要: 目的 探讨脂联素对子宫内膜癌细胞增殖侵袭及 PI3K / AKT / NF-κB 通路蛋白质活化的影响方法 子宫内膜癌细胞系 AN3CA HEC-1-A 转染 pcDNA、 pcDNA-脂联素。 RT-PCR 和蛋白质印迹检测脂联素过表达效率细胞计数试剂盒-8 (cell counting kit-8, CCK-8) 检测细胞增殖, 流式细胞术检测细胞凋亡率, Transwell 小室检测侵袭, 蛋白质印迹检测半胱氨酸蛋白酶 9 ( caspase-9 )、 半胱氨酸蛋白酶 3(caspase-3)、 血管内皮生长因子 (vascular endothelial growth factor, VEGF)、 E-钙黏蛋白 (E-cadherin)、 N-钙黏蛋白 (N-cadherin)、 纤维粘连蛋白 ( fibronectin, FN)、 磷脂酰肌醇 3-激酶 ( phosphatidylinositol 3-kinase, PI3K) 及其磷酸化形式 (p-PI3K)、 蛋白激酶 B (protein kinase B, AKT) 及其磷酸化形式 (p-AKT)、核因子 κB P65 亚基 (nuclear factor kappa B p65 subunit, P65) 及其磷酸化形式 (p-P65) 的蛋白质水平结果 Control 组比较, AN3CA HEC-1-A 细胞中脂联素表达水平明显增高 ( P< 0. 05), 细胞增殖倍数显著降低 ( P < 0. 05), 细胞凋亡率显著增多 ( P < 0. 05), 细胞侵袭数显著减少 ( P < 0. 05), caspase-9 caspase-3 蛋白水平显著上调 (P< 0. 05), VEGF 蛋白质水平显著下调 (P< 0. 05), E-cadherin 蛋白质水平增高, N-cadherin FN 蛋白质水平降低 (P< 0. 05), PI3K / AKT / P65 磷酸化蛋白质水平显著降低 (P< 0. 05)。结论 脂联素抑制子宫内膜癌细胞 AN3CA HEC-1-A 增殖侵袭及 PI3K / AKT / NF-κB 通路蛋白质的活化

关键词: 脂联素, 子宫内膜癌, PI3K / AKT / NF-κB 通路

Abstract: Objective To explore the effect of adiponectin on the proliferation, invasion, andphosphatidylinositol 3-kinase / protein kinase B / nuclear factor kappa B (PI3K / AKT / NF-κB) pathway in endometrial cancer cells. Methods Endometrial cancer cell lines AN3CA and HEC-1-Awere transfected with pcDNA, pcDNA-adiponectin. The efficiency of adiponectin overexpression were detected by RT-PCR and Western blotting. Cell proliferation, cell apoptosis, and cell invasion were detected by CCK8, flow cytometry, and Transwell assay, respectively. The expression levels of caspase-9, caspase-3, vascular endothelial growth factor ( VEGF), E-cadherin, N-cadherin, fibronectin ( FN ), p-PI3K / PI3K, p-AKT / AKT, p-P65 / P65 were detected by Western blotting. Results Compared with those in the Control group, the adiponectin expression levels of endometrial cancer cells AN3CA and HEC-1-A in the adiponectin group were significantly increased(P < 0. 05), the cell proliferation ratio was significantly reduced (P < 0. 05), and the rate of apoptosis was significant increase (P < 0. 05), cell invasion number was significantly reduced (P <0. 05), the expression levels of caspase-9 and caspase-3 were significantly increased (P < 0. 05),VEGF levels were significantly decreased (P< 0. 05), E-cadherin level was increased, N-cadherinand FN levels were decreased (P< 0. 05), phosphorylated PI3K / AKT / P65 levels were significantly decreased (P< 0. 05). Conclusion Adiponectin inhibits the proliferation and invasion of endometrial cancer AN3CA and HEC-1-A cells and the activation of PI3K / AKT / NF-κB pathway.

Key words: adiponectin, endometrial cancer, PI3K / AKT / NF-κB pathway

中图分类号: