地佐辛调节p38MAPK/JNK信号通路对子宫内膜癌细胞增殖侵袭凋亡等影响

doi:10.3969/j.issn.1006-6233.2025.12.02

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摘要 目的: 探讨地佐辛(Dez)调节p38丝裂原活化蛋白激酶38(p38MAPK)/c-Jun氨基末端激酶(JNK)信号通路对子宫内膜癌(UCEC)细胞增殖、凋亡和上皮间质转化的影响。方法: 体外培养人UCEC细胞HEC-1A,随机分为NC组、Dez低剂量、Dez中剂量、Dez高剂量组(2.5、5、10μg/mL Dez)、Dez高剂量+SB203580组(10μg/mL Dez+10μmoL/L p38MAPK抑制剂SB203580)。MTS法检测HEC-1A细胞增殖;平板克隆法检测HEC-1A细胞克隆形成能力;流式细胞仪检测HEC-1A细胞凋亡;Transwell实验检测HEC-1A细胞侵袭情况;Western blot检测E-cadherin、N-cadherin、Snail及p38MAPK/JNK信号通路蛋白表达情况。结果: 与NC组相比,Dez低剂量组、Dez中剂量组、Dez高剂量组中HEC-1A细胞的D(λ)490_nm、克隆形成率、细胞侵袭数、N-cadherin、Snail蛋白表达降低,凋亡率、E-cadherin、p-p38MAPK/p38MAPK、p-JNK/JNK蛋白表达升高(P<0.05);与Dez高剂量组相比,Dez高剂量+SB203580组HEC-1A细胞的D(λ)490_nm、克隆形成率、细胞侵袭数、N-cadherin、Snail蛋白表达升高,凋亡率、E-cadherin、p-p38MAPK/p38MAPK、p-JNK/JNK蛋白表达降低(P<0.05)。结论: Dez具有抑制UCEC细胞增殖、侵袭及及上皮间质转化,促进UCEC细胞凋亡等的作用,这可能是通过激活p38MAPK/JNK信号通路实现的。

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	李传进
	曹晓霞
	丁章俊

关键词 ：子宫内膜癌, 地佐辛, p38丝裂原活化蛋白激酶38/c-Jun氨基末端激酶, 细胞增殖, 细胞凋亡, 上皮间质转化

Abstract：Objective: To explore the effects of dezocine (Dez) on the proliferation, apoptosis, and epithelial-mesenchymal transition of uterine corpus endometrial cancer (UCEC) cells by regulating p38 mitogen-activated protein kinase 38 (p38MAPK)/c-Jun N-terminal kinase (JNK) signaling pathway. Methods: Human UCEC cells HEC-1A were cultured in vitro and randomly assigned into NC group, low-dose Dez group, medium-dose Dez group, high-dose Dez group (2.5, 5, 10μg/mL Dez), and high-dose Dez+SB203580 group (10μg/mL Dez+10μmol/L p38MAPK inhibitor SB203580). MTS method was used to detect the proliferation of HEC-1A cells. The plate cloning method was used to measure the clonogenic ability of HEC-1A cells. Flow cytometry was used to measure apoptosis of HEC-1A cells. Transwell experiment was used to detect the invasion of HEC-1A cells. Western blot was used to measure the E-cadherin, N-cadherin, Snail, and p38MAPK/JNK signaling pathway proteins. Results: For the NC group, the low-dose, medium-dose, and high-dose Dez groups showed a decrease in D(λ)490_nm, colony formation rate, cell invasion number, N-cadherin, and Snail proteins in HEC-1A cells, and an increase in apoptosis rate, E-cadherin, p-p38MAPK/p38MAPK, and p-JNK/JNK proteins (P<0.05). For the high-dose Dez group, the high-dose Dez+SB203580 group showed an increase in D(λ)490_nm, colony formation rate, cell invasion number, N-cadherin, and Snail proteins in HEC-1A cells, and a decrease in apoptosis rate, E-cadherin, p-p38MAPK/p38MAPK, and p-JNK/JNK proteins (P<0.05). Conclusion: Dez exerts inhibitory effects on the proliferation, invasion, and epithelial mesenchymal transition of UCEC cells, while promoting UCEC cells apoptosis. This is likely mediated through activating the p38MAPK/JNK signaling pathway.

Key words： Endometrial cancer Dezocine P38 mitogen activated protein kinase 38/c-Jun N-terminal kinase Cell proliferation Cell apoptosis Epithelial mesenchymal transition

基金资助:湖北省卫生健康委科研项目,(编号:WJ2023M117)

引用本文:

李传进, 曹晓霞, 丁章俊. 地佐辛调节p38MAPK/JNK信号通路对子宫内膜癌细胞增殖侵袭凋亡等影响[J]. 河北医学, 2025, 31(12): 1943-1949.
LI Chuanjin, CAO Xiaoxia, DING Zhangjun. Effect of Dezocine on the Proliferation Invasion and Apoptosis of Endometrial Carcinoma Cells via Regulating p38MAPK/JNK Signaling Pathway. HeBei Med, 2025, 31(12): 1943-1949.

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http://www.hbyxzzs.cn/CN/10.3969/j.issn.1006-6233.2025.12.02 或 http://www.hbyxzzs.cn/CN/Y2025/V31/I12/1943

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