和厚朴酚通过调节ATF4/CHOP/TRIB3通路抑制胃癌细胞恶性进程OA
Honokiol inhibits the malignant progression of gastric cancer cells by regulating the ATF4/CHOP/TRIB3 pathway
目的 探讨和厚朴酚(Honokiol)对胃癌细胞增殖、凋亡、迁移和侵袭的影响及其潜在机制.方法 选取0、15、25 μmol/L Honokiol处理人胃癌细胞系HGC-27与AGS.CCK-8检测两株细胞的半抑制浓度(IC50);CCK-8、克隆形成、划痕、Transwell迁移及Transwell侵袭实验检测细胞存活率、增殖、迁移、侵袭能力;流式细胞术检测细胞凋亡率;Western blot检测增殖、凋亡、迁移、侵袭及内质网应激通路ATF4-CHOP-TRIB3的相关蛋白.结果 与对照组比较,15、25 μmol/L Honokiol处理后两株胃癌细胞的增殖、克隆形成、迁移和侵袭能力明显降低,凋亡率明显升高(P<0.05);与对照组比较,15、25 μmol/L Honokiol处理后两株胃癌细胞的神经钙黏蛋白(N-cadherin)、波形蛋白(Vimentin)、增殖细胞核抗原(PCNA)、B细胞淋巴瘤/白血病-2蛋白(Bcl-2)表达下降,上皮钙黏蛋白(E-cadherin)、Bcl-2相关X蛋白(Bax)、转录激活因子4(ATF4)、内质网应激相关蛋白(CHOP)、Tribbles同源蛋白3(TRIB3)表达上升(P<0.05).结论 Honokiol通过调节内质网应激信号通路ATF4/CHOP/TRIB3促进胃癌细胞HGC-27、AGS凋亡,抑制其增殖、迁移和侵袭.
Objective To investigate the effect of honokiol on proliferation,apoptosis,migration,and invasion of gastric cancer cells and its underlying mechanistic.Methods Human gastric cancer cell lines HGC-27 and AGS were treated with Honokiol at concentrations of 0,15,and 25 μmol/L.CCK-8 assays were conducted to determine the half maximal inhibitory concentration(IC50)for both cell lines.Cell viability,proliferation,migration,and in-vasion capabilities were assessed using CCK-8,colony formation,wound healing,Transwell migration and Tran-swell invasion assays.Apoptosis rates were measured via flow cytometry.Western blot analysis examined proteins related to proliferation,apoptosis,migration,invasion,and the endoplasmic reticulum stress pathway ATF4-CHOP-TRIB3.Results Compared with the control group,treatment with 15 and 25 μmol/L Honokiol significantly reduced the proliferation,colony formation,migration,and invasion capabilities of the two gastric cancer cell lines,while significantly increasing the apoptosis rate(P<0.05).Additionally,compared to the control group,the protein expression levels of neural cadherin(N-cadherin),Vimentin,proliferating cell nuclear antigen(PCNA),and B-cell lymphoma/leukemia-2 protein(Bcl-2)decreased in the two gastric cancer cell lines after treat-ment with 15 and 25 μmol/L Honokiol,while the protein expression levels of epithelial cadherin(E-cadherin),Bcl-2-associated X protein(Bax),activating transcription factor 4(ATF4),endoplasmic reticulum stress-related pro-tein(CHOP),and tribbles homolog 3(TRIB3)increased(P<0.05).Conclusion Honokiol promotes apoptosis and inhibits proliferation,migration,and invasion of gastric cancer HGC-27 and AGS cells by regulating the ERS sig-naling pathway ATF4/CHOP/TRIB3.
代凯红;文贤慧;黄赟;韦四喜;黄海
贵州医科大学附属医院临床检验中心,贵阳 550004||贵州医科大学检验学院,贵阳 550004贵州医科大学附属医院临床检验中心,贵阳 550004||贵州医科大学检验学院,贵阳 550004贵州医科大学附属医院临床检验中心,贵阳 550004||贵州医科大学检验学院,贵阳 550004贵州医科大学附属医院临床检验中心,贵阳 550004||贵州医科大学检验学院,贵阳 550004贵州医科大学附属医院临床检验中心,贵阳 550004||贵州医科大学检验学院,贵阳 550004
医药卫生
和厚朴酚胃癌内质网应激ATF4/CHOP/TRIB3信号通路凋亡靶向
honokiolgastric cancerendoplasmic reticulum stressATF4/CHOP/TRIB3 signaling pathwayapoptosistargeting
《安徽医科大学学报》 2026 (5)
827-835,9
国家自然科学基金项目(编号:82560798)贵州省卫生健康委科学技术基金项目(编号:gzwjkj2020-1-242) National Natural Science Foundation of China(No.82560798)Scientific and Technological Project of Guizhou Health Commission(No.gzwkj2020-1-242)
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