基于AMPK-ACC信号通路探究miR-543对肺癌细胞放疗敏感性的机制研究  

The Mechanism of miR-543 on Radiosensitivity in Lung Cancer Cells Based on AMPK-ACC Signaling Pathway

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作  者:储祥健 曹海燕 戴美云[1] CHU Xiangjian;CAO Haiyan;DAI Meiyun(Rugao People's Hospital,Jiangsu Rugao 226500,China)

机构地区:[1]江苏省如皋市人民医院,江苏如皋226500

出  处:《河北医学》2023年第7期1068-1074,共7页Hebei Medicine

基  金:江苏省优势学科建设工程项目,(编号:YSHL0814-789)。

摘  要:目的:放射抗性是非小细胞肺癌(Non-small cell lung carcinoma,NSCLC)放疗的一个重要障碍。据报道,miR-543在包括NSCLC在内的各种类型的癌症中是一种肿瘤促进因子。本研究旨在探索miR-543在调节NSCLC细胞放射敏感性中的潜在作用。方法:qRT-PCR检测miR-543的表达;CCK8、集落形成实验和流式细胞术等手段探究miR-543对NSCLC细胞生物学功能的影响。WB检测AMPK-ACC信号通路相关蛋白的表达。利用回复实验和辐射处理实验进一步验证miR-543通过AMPK-ACC信号通路对NSCLC细胞的恶性进展和放疗抗性的影响。结果:miR-53在NSCLC组织和细胞中均表达上调。沉默miR-53可以抑制NSCLC细胞的增殖能力,促进细胞周期阻滞和凋亡的发生,减弱放疗抗性。此外,miR-53参与调控AMPK-ACC信号通路,而使用compound C(AMPK-ACC信号通路的抑制剂)可以减弱miR-53沉默对NSCLC细胞行为及放疗敏感性的影响。结论:本研究的结果表明,miR-53可以通过调控AMPK-ACC信号通路增强NSCLC细胞的放疗抗性的机制,提示靶向miR-53可能是改善NSCLC的放射治疗敏感性的潜在治疗靶点。Objective:To explore the potential role of miR-543 in regulating the radiosensitivity of NSCLC cells.Methods:The expression of miR-543 was detected by qRT-PCR;CCK8,colony formation assay and flow cytometry were used to explore the effect of miR-543 on the biological function of NSCLC cells.The expression of proteins related to AMPK-ACC signaling pathway was detected by WB.Reversion experiments and radiation treatment experiments were used to further verify the effect of miR-543 on the malignant progression and radiotherapy resistance of NSCLC cells through the AMPK-ACC signaling pathway.Results:miR-53 was up-regulated in NSCLC tissues and cells.Silencing miR-53 can inhibit the proliferation ability of NSCLC cells,promote cell cycle arrest and apoptosis,and weaken radiotherapy resistance.In addition,miR-53 is involved in the regulation of AMPK-ACC signaling pathway,and the use of compound C(an inhibitor of AMPK-ACC signaling pathway)can attenuate the effect of miR-53 silencing on NSCLC cell behavior and radiosensitivity.Conclusion:The results of this study suggest that miR-53 can enhance the radiotherapy resistance mechanism in NSCLC cells by regulating the AMPK-ACC signaling pathway,suggesting that targeting miR-53 may be a potential therapeutic target to improve the radiotherapy sensitivity in NSCLC.

关 键 词:miR-543 非小细胞肺癌 放疗抗性 AMPK-ACC信号通路 

分 类 号:R734.2[医药卫生—肿瘤]

 

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