METTL3通过上调ING5抑制非小细胞肺癌细胞增殖

目的:探讨METTL3在非小细胞肺癌中的表达及作用,并探讨其可能的机制。方法:通过慢病毒转染,在HCC827细胞中过表达和敲除METTL3,并通过免疫印迹验证METTL3蛋白表达。免疫印迹检测HCC827细胞中生长抑制物家族成5(Methyltransferase Like 3,甲基转移酶3)调控ING5(Inhibitor Of Growth Family Member 5,METTL3)。使用基因表达交互分析(Gene Expression Profiling Interactive Analysis,GEPIA)探究了METTL3和ING5在非小细胞肺癌组织和正常组织中的表达相关性。用CCK-8法检测METTL3和ING5表达对非小细胞肺癌细胞增殖的影响。使用KM-plotter验证METTL3、ING5的表达与非小细胞肺癌的总生存期(OS)、进展后生存期(PPS)和无进展生存期(PFS)之间的相关性。结果:免疫印迹结果显示,在HCC827细胞中METTL3过表达上调了ING5蛋白的表达,而METTL3表达下调了ING5蛋白的表达。GEPIA数据库分析显示METTL3在非小细胞肺癌中的表达明显低于正常组织(P<0.05)。CCK-8检测结果显示,与对照组相比METTL3缺失促进了HCC827细胞的增殖能力,而METTL3过表达显著抑制了HCC827细胞的增殖能力。此外,METTL3通过ING5调控非小细胞肺癌细胞的增殖能力。KM-plotter分析显示METTL3、ING5 m RNA的表达与非小细胞肺癌患者的生存有较好的预后关系。结论:METTL3在非小细胞肺癌低表达,并通过调控ING5的表达在非小细胞肺癌的发生进展中发挥重要地抑癌基因作用。

METTL3 Inhibited Proliferation of Non-small Cell Lung Cancer Cells by Targeting ING5

Objective: To determine the expression level and effect of METTL3 in the Non-small cell lung cancer(NSCLC,Non-small cell lung cancer), and explore the potential mechanism. Methods: Lentivirus transfection were used to overexpress and knockdown METTL3 in HCC827 cells, and western blot was used to validate the METTL3 protein expression. METTL3 regulated ING5 in HCC827 cells was detected by Western blot. GEPIA was used to analyze the expression correlation of METTL3 and ING5 in NSCLC tissues and normal tissues. The effect of METTL3 and ING5 expression on the proliferation of NSCLC cells was detected by CCK-8 assay. KM-plotter was used to validate the correlation between the expression of METTL3 and the overall survival(OS), post-progression survival(PPS), and progression-free survival(PFS) of NSCLC. Results: Western blot show that METTL3 overexpression in HCC827 cells upregulated ING5 protein levels, whereas METTL3 knockdown decreased ING5 protein expression. Analysis of GEPIA database indicated that METTL3 expression was significantly lower in NSCLC than in normal tissues(P<0.05). CCK-8 assay showed that,compared to in control cells, METTL3 depletion promotedHCC827 cell proliferation ability and its overexpression significantly inhibited cell proliferation ability. Moreover, ING5 overexpression rescued the anti-tumor phenotype impaired by METTL3 knockdown.KM-plotter analysis showed that the better prognostic relationship between METTL3 m RNA expression and the survival of patients with NSCLC. Conclusions: METTL3 was low expressed in NSCLC, and played an important anti-cancer role in inhibiting the development of NSCLC by regulating the expression of ING5.