Abstract：
UNASSIGNED: N6-methyladenosine (m6A) of RNA is involved in the progression of non-small cell lung cancer (NSCLC).
UNASSIGNED: This study investigated the role of METTL14 in NSCLC and the mechanism.
UNASSIGNED: Expression levels were assessed by quantitative real-time PCR and ELISA assays. Cells viability was assessed by cell counting kit-8. M6A methylation was analysed by methylated RNA immunoprecipitation (MeRIP), RIP, luciferase assay, and mRNA stability assay.
UNASSIGNED: The results showed that METTL14 was highly expressed in NSCLC tissues and cell lines. Knockdown of METTL14 inhibited the cell viability while induced ferroptosis of NSCLC cells. Mechanistically, METTL14 interacts with GPX4, mediates m6A modification of GPX4, enhances its mRNA stability, and upregulates its expression. In addition, IGF2BP1 recognises the m6A-methylated GPX4 and mediates the elevated mRNA stability. Moreover, GPX4 reversed the effects of METTL14 depletion.
UNASSIGNED: The METTL14/GPX4 axis promotes NSCLC progression by inhibiting cell ferroptosis through the recognition of m6A modification mediated by IGF2BP1.
UNASSIGNED: This study investigated the role of METTL14 in NSCLC and the mechanism.
UNASSIGNED: Expression levels were assessed by quantitative real-time PCR and ELISA assays. Cells viability was assessed by cell counting kit-8. M6A methylation was analysed by methylated RNA immunoprecipitation (MeRIP), RIP, luciferase assay, and mRNA stability assay.
UNASSIGNED: The results showed that METTL14 was highly expressed in NSCLC tissues and cell lines. Knockdown of METTL14 inhibited the cell viability while induced ferroptosis of NSCLC cells. Mechanistically, METTL14 interacts with GPX4, mediates m6A modification of GPX4, enhances its mRNA stability, and upregulates its expression. In addition, IGF2BP1 recognises the m6A-methylated GPX4 and mediates the elevated mRNA stability. Moreover, GPX4 reversed the effects of METTL14 depletion.
UNASSIGNED: The METTL14/GPX4 axis promotes NSCLC progression by inhibiting cell ferroptosis through the recognition of m6A modification mediated by IGF2BP1.
摘要：
■RNA的N6-甲基腺苷(m6A)参与非小细胞肺癌(NSCLC)的进展。
■本研究探讨了METTL14在非小细胞肺癌中的作用及其机制。
通过定量实时PCR和ELISA测定评估表达水平。通过细胞计数试剂盒-8评估细胞活力。通过甲基化RNA免疫沉淀（MeRIP）分析M6A甲基化，RIP,荧光素酶测定,和mRNA稳定性测定。
■结果表明，METTL14在NSCLC组织和细胞系中高表达。敲除METTL14抑制细胞活力，同时诱导NSCLC细胞的铁凋亡。机械上,METTL14与GPX4相互作用，介导GPX4的m6A修饰，增强其mRNA稳定性，并上调其表达。此外,IGF2BP1识别m6A甲基化的GPX4并介导提高的mRNA稳定性。此外，GPX4逆转了METTL14耗尽的影响。
■METTL14/GPX4轴通过识别IGF2BP1介导的m6A修饰抑制细胞铁性凋亡促进NSCLC进展。
■本研究探讨了METTL14在非小细胞肺癌中的作用及其机制。
通过定量实时PCR和ELISA测定评估表达水平。通过细胞计数试剂盒-8评估细胞活力。通过甲基化RNA免疫沉淀（MeRIP）分析M6A甲基化，RIP,荧光素酶测定,和mRNA稳定性测定。
■结果表明，METTL14在NSCLC组织和细胞系中高表达。敲除METTL14抑制细胞活力，同时诱导NSCLC细胞的铁凋亡。机械上,METTL14与GPX4相互作用，介导GPX4的m6A修饰，增强其mRNA稳定性，并上调其表达。此外,IGF2BP1识别m6A甲基化的GPX4并介导提高的mRNA稳定性。此外，GPX4逆转了METTL14耗尽的影响。
■METTL14/GPX4轴通过识别IGF2BP1介导的m6A修饰抑制细胞铁性凋亡促进NSCLC进展。
