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首页> 外文期刊>Journal of cellular biochemistry. >Downregulation of miR-33b promotes non-small cell lung cancer cell growth through reprogramming glucose metabolism miR-33b regulates non-small cell lung cancer cell growth
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Downregulation of miR-33b promotes non-small cell lung cancer cell growth through reprogramming glucose metabolism miR-33b regulates non-small cell lung cancer cell growth

机译:MiR-33B的下调通过重编程葡萄糖代谢miR-33b调节非小细胞肺癌细胞生长的非小细胞肺癌细胞生长

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摘要

Glucose metabolism is a common target for cancer regulation and microRNAs (miRNAs) are important regulators of this process. Here we aim to investigate a tumor-suppressing miRNA, miR-33b, in regulating the glucose metabolism of non-small cell lung cancer (NSCLC). In our study, quantitative real-time polymerase chain reaction (qRT-PCR) showed that miR-33b was downregulated in NSCLC tissues and cell lines, which was correlated with increased cell proliferation and colony formation. Overexpression of miR-33b through miR-33b mimics transfection suppressed NSCLC proliferation, colony formation, and induced cell-cycle arrest and apoptosis. Meanwhile, miR-33b overexpression inhibited glucose metabolism in NSCLC cells. Luciferase reporter assay confirmed that miR-33b directly binds to the 3 '-untranslated region of lactate dehydrogenase A (LDHA). qRT-PCR and Western blot analysis showed that miR-33b downregulated the expression of LDHA. Moreover, introducing LDHA mRNA into cells over-expressing miR-33b attenuated the inhibitory effect of miR-33b on the growth and glucose metabolism in NSCLC cells. Taken together, these results confirm that miR-33b is an anti-oncogenic miRNA, which inhibits NSCLC cell growth by targeting LDHA through reprogramming glucose metabolism.
机译:葡萄糖代谢是癌症调节的常见目标,MicroRNA(miRNA)是该过程的重要调节因素。在这里,我们的目的是探讨肿瘤抑制miRNA,miR-33b,用于调节非小细胞肺癌(NSCLC)的葡萄糖代谢。在我们的研究中,定量实时聚合酶链反应(QRT-PCR)显示MIR-33B在NMSCLC组织和细胞系中下调,其与细胞增殖和菌落形成的增加相关。 MiR-33B通过miR-33b模拟转染的过表达抑制了Nsclc增殖,菌落形成和诱导的细胞周期停滞和细胞凋亡。同时,miR-33b过表达抑制了Nsclc细胞中的葡萄糖代谢。荧光素酶报告器测定证实,miR-33b直接与乳酸脱氢酶A(LDHA)的3' - 次转移区域结合。 QRT-PCR和Western印迹分析表明miR-33b下调了LDHA的表达。此外,将LDHA mRNA引入细胞过度表达miR-33b衰减miR-33b对NSCLC细胞中生长和葡萄糖代谢的抑制作用。总之,这些结果证实miR-33b是一种抗致癌miRNA,其通过通过重编程葡萄糖代谢来靶向LDHA来抑制NSCLC细胞生长。

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