METTL3介导 m6A 修饰lncRNASNHG5对骨肉瘤MG-63细胞增殖和侵袭的影响
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【中图分类号】R738 【文献标志码】A
【Abstract】Objective：To investigate the expression of m6A methyltransferase-like protein 3（METTL3） in human osteosarcoma（OS） tisue and theefectofMETTL3ontheproliferationand invasionofMG-63cels.Methods：QuantitativePCRand Westerblottig wereusedtomeasuretheexpressonlevelofMETTL3in5pairsofhumanOStissesamplesandinvestigate theefectofMETTL3on the downstream long non-coding RNA（lncRNA） small nucleolar RNA host gene 5（SNHG5） and the Wnt/β -catenin signaling pathway;methylatedRNAimmunoprecipitationwasusedtoobservetheefectofMETTL3knockdownonthemAleveloflncRNASNHG5; CCK-8 assayand Transwellassaywereusedtomeasurecellproliferationandinvasion；Western bloting wasused tomeasurethe change in the activity of the Wnt/β -catenin signaling pathway.Results ：Compared with the paracancerous normal tissue，human OS tissue showed significant increases in the mRNA and protein expression levels of METTL3（ P =0.034 and 0.002），and knockdown of METTL3 reduced the m6A level and mRNA expression level of lncRNA SNHG5（ P =0.027 and 0.0o2）.Functionally，knockdownof METTL3 inhibited the proliferation and invasion of MG-63 cells（ P =0.014 and O.0O1） and the protein expression levels of Wnt1， Wnt3a，Wnt1Oa，β-catenin，and C-myc（all P<0.01 ），while overexpression of SNHG5 promoted cell proliferation（ P =0.027）and invasion （ P=0.006 ），activated the Wnt/β -catenin signaling pathway（ P <0.01），and reversed the antitumor effect induced by METTL3 knockdown（ P<0.01 ）.Conclusion：METTL3-mediated m6A modification of lncRNA SNHG5 promotes the proliferation and invasion of
MG-63 cells by activating the Wnt/β-catenin signaling. 【Keywords】methyltransferase-like protein 3；long non-coding RNA small nucleolar RNA host gene5;osteosarcoma;proliferation; invasion
骨肉瘤是儿童和青少年最常见的原发性骨恶性肿瘤，占所有骨恶性肿瘤的 50% 以上。（剩余7412字）
