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作 者:高可欣 李文媛[1] 赵微 邹明明 欧津瑞 孙平 GAO Kexin;LI Wenyuan;ZHAO Wei;ZOU Mingming;OU Jinrui;SUN Ping(Department of Anatomy,School of Basic Medicine,Mudanjiang Medical University,Heilongjiang Mudanjiang 157011,China)
机构地区:[1]牡丹江医学院基础医学院解剖教研室,黑龙江牡丹江157011
出 处:《现代肿瘤医学》2024年第8期1424-1429,共6页Journal of Modern Oncology
基 金:黑龙江省基本科研业务费项目(编号:2022-KYYWF-0704);黑龙江省牡丹江市应用技术研究与开发计划(编号:HT2022JG133);牡丹江医学院导师科研专项计划(编号:YJSZX2022011)。
摘 要:目的:研究TNF-α对乳腺癌MCF-7细胞中LRG1蛋白表达的调控及其对乳腺癌MCF-7细胞增殖、侵袭和迁移能力的影响及相关分子机制。方法:MTT实验检测不同浓度TNF-α处理后MCF-7细胞活力;EdU实验、Transwell实验和划痕实验分别检测抑制LRG1表达后细胞增殖、侵袭以及迁移能力;Western blot检测细胞内MAPK信号通路中p-p38蛋白表达。结果:低浓度TNF-α处理乳腺癌MCF-7细胞,细胞活力增强;抑制LRG1表达后细胞增殖能力下降,侵袭细胞数、细胞迁移率以及p-p38蛋白表达均下降。结论:TNF-ɑ通过调控LRG1的表达促进乳腺癌MCF-7细胞增殖、侵袭和迁移,这一过程可能通过激活p38MAPK信号通路来实现。Objective:To investigate the regulation of LRG1 protein expression by TNF-α in breast cancer MCF-7 cells and its effects on the proliferation,invasion and migration ability of MCF-7 cells.Methods:MTT assay was used to detect the viability of MCF-7 cells treated with different concentrations of TNF-α.Cell proliferation,invasion and migration capacity was assessed by EdU,Transwell and scratch experiments,respectively after inhibiting the expression of LRG1.Western blot was used to detect p-p38 protein expression in intracellular MAPK signaling pathway.Results:Breast cancer MCF-7 cells treated with low concentrations of TNF-α showed enhanced cell viability.Cell proliferation ability was decreased after inhibition of LRG1 expression.The number of invasive cells,migration rate and p-p38 protein expression were also decreased.Conclusion:TNF-ɑ promotes the proliferation,invasion,and migration of breast cancer MCF-7 cells by regulating LRG1 expression and this process may be achieved through the activation of the p38MAPK signaling pathway.
关 键 词:TNF-ɑ LRG1 P38MAPK 乳腺癌MCF-7细胞
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