医学分子生物学杂志 ›› 2024, Vol. 21 ›› Issue (4): 354-360.doi: 10.3870/j.issn.1672-8009.2024.04.010

• 论著 • 上一篇    下一篇

基于 PI3K / AKT 信号通路研究山柰酚在食管鳞癌中的抗肿瘤作用 #br#

  

  1. 1西安国际医学中心医院胸外科 西安市, 710075 2广州中医药大学中医科 广州市, 510006
  • 出版日期:2024-07-31 发布日期:2024-09-09
  • 基金资助:
    陕西省重点研发计划项目 (No. 2022SF-325)

Anti-Tumor Effect of Kaempferol on Esophageal Squamous Cell Carcinoma through PI3K / AKT Signaling Pathway #br#

  1. 1Department of Thoracic Surgery, Xian International Medical Center Hospital, Xian, 710075, China 2Department of Traditional Chinese Medicine, Guangzhou University of Traditional Chinese Medicine, Guangzhou, 510006, China
  • Online:2024-07-31 Published:2024-09-09

摘要: 目的 探究山柰酚对食管鳞癌 (esophageal squamous cell carcinoma, ESCC) 的抗肿瘤作用和潜在机制方法 通过 CCK-8、 集落形成和流式细胞术测定山柰酚对 ECA-109 细胞系增殖和凋亡的影响; Transwell 实验检测细胞侵袭; 蛋白质印迹检测相关蛋白表达水平结果 与山柰酚 0 μmol / L 组相比, 山柰酚40 μmol / L 60 μmol / L 明显抑制了 ECA-109 细胞的增殖侵袭能力, 并诱导其凋亡与山柰酚 0 μmol / L组相比, 山柰酚 40 μmol / L 60 μmol / L 显著降低增殖细胞核抗原 (proliferating cell nuclear antigen, PCNA)Ki67 的表达, 且抑制磷脂酰肌醇 3-激酶 (phosphatidylin-ositol-3-kinase, PI3K) 和蛋白激酶 B (protein kinase B, AKT) 蛋白的磷酸化水平, 并增加了促凋亡相关蛋白的表达水平此外, PI3K 激活剂 740Y-P 逆转了山柰酚对 ECA-109 细胞增殖侵袭和凋亡的调控作用结论 山柰酚通过抑制 PI3K / AKT 信号通路来抑制 ECA-109 细胞的增殖侵袭和诱导凋亡

关键词: 山柰酚, 食管鳞癌, 凋亡, 侵袭, PI3K / AKT

Abstract: Objective To investigate the anti-tumor effect and potential mechanism ofkaempferol on esophageal squamous cell carcinoma (ESCC) cells. Methods CCK-8, colony formation and flow cytometry were used to determine the effect of kaempferol on the proliferation andapoptosis of ECA-109 cells. Transwell assay was used to detect cell invasion. Western blotting wasemployed to measure the protein expression levels. Results Compared with the 0 μmol / L kaempferol group, the 40 μmol / L and 60 μmol / L kaempferol groups had significantly inhibited proliferationand invasion of ECA-109 cells and enhanced apoptosis. Moreover, kaempferol (40 μmol / L and 60μmol / L ) had significantly decreased expression levels of proliferating cell nuclear antigen (PCNA) and Ki67, and lower phosphorylation levels of phosphatidylin-ositol-3-kinase ( PI3K) and protein kinase B ( AKT), and increased expression levels of pro-apoptosis-related proteins. In addition, PI3K activator 740Y-P reversed the regulatory effect of kaempferol on proliferation, invasion and apoptosis of ECA-109 cells. Conclusion Kaempferol inhibits the proliferation, invasion and inducesthe apoptosis of ECA-109 cells by inhibiting PI3K / AKT signaling pathway.

Key words:

kaempferol, esophageal squamous cell carcinoma, apoptosis, invasion, PI3K / AKT


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