首页> 外文期刊>OncoTargets and therapy >MicroRNA-647 promotes the therapeutic effectiveness of argon–helium cryoablation and inhibits cell proliferation through targeting TRAF2 via the NF-κB signaling pathway in non-small cell lung cancer
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MicroRNA-647 promotes the therapeutic effectiveness of argon–helium cryoablation and inhibits cell proliferation through targeting TRAF2 via the NF-κB signaling pathway in non-small cell lung cancer

机译:MicroRNA-647促进氩链氦光滑的治疗效果,并通过非小细胞肺癌中的NF-κB信号传导途径靶向TRAF2,抑制细胞增殖

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Background: MicroRNA-647 (miR-647) has been reported to repress cell tumorigenic phenotype, while the function of miR-647 in non-small cell lung cancer was obscure. Methods: The effect of miR-647 and TRAF2 on A549 and H1299 cells was explored through Methyl thiazolyl tetrazolium (MTT) assay, colony formation and cell cycle assays. Luciferase reporter assays, reverse transcription quantitative PCR (RT-qPCR) and Western blot assay were carried out to determine that TRAF2 is directly regulated by miR-647. The effect of miR-647/ TRAF2 axis on p65 protein level in nucleus or total was detected by Western blot assay. Results: Here, we found that miR-647 was high expression in tumor that under argon-helium cryoablation treatment in contrast to the tumor under non argon-helium cryoablation treatment and inhibited cell proliferation of A549 and H1299 cells by inducing G1-S transition. TRAF2 was confirmed as a target of miR-647. TRAF2 overexpression partially rescued the suppressive function of miR-647 in A549 and H1299 cells. Moreover, we found that miR-647 repressed lung carcinogenesis by attenuating NF-κB pathway. Conclusion: In all, our study demonstrates that miR-647 functions as tumor suppressor via targeting and down-regulating the expression of TRAF2 and NF-κB signaling pathway in non-small cell lung cancer.
机译:背景:据报道,MicroRNA-647(miR-647)抑制细胞致瘤表型,而MIR-647在非小细胞肺癌中的功能是模糊的。方法:通过甲基唑氧基四唑(MTT)测定,菌落形成和细胞周期测定探索MIR-647和TRAF2对A549和H1299细胞的影响。荧光素酶报告器测定,逆转录定量PCR(RT-QPCR)和蛋白质印迹测定进行,以确定TRAF2由miR-647直接调节。通过Western印迹测定检测miR-647 / Traf2轴对核或总量的P65蛋白水平的影响。结果:在这里,我们发现miR-647在肿瘤中是高表达,在氩氦低温处理下,与非氩链氦低温处理的肿瘤相比,通过诱导G1-S转变抑制A549和H1299细胞的细胞增殖。 TRAF2被证实为MIR-647的目标。 TRAF2过表达部分拯救了A549和H1299细胞中miR-647的抑制功能。此外,我们发现MiR-647通过衰减NF-κB途径来压抑肺癌。结论:全部,我们的研究表明,MIR-647通过靶向和下调非小细胞肺癌中的TRAF2和NF-κB信号传导途径的表达和降低肿瘤抑制剂。

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