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mettl, cells, luad, slca, cell, pubmed, cancer, ferroptosis, fig, google, scholar, knockdown, rna, expression, ythdf, mrna, cas, modification, lung, overexpression, central, analysis, zhang, levels, showed, protein, tumor, patients, ihc, progression, level, mettlmediated, control, data, growth, translation, chen, wang, stability, role, proliferation, found, liu, assays, western, blot, promotes, adenocarcinoma, apoptosis, effect,

Topics {✒️}

tgf-β-induced epithelial-mesenchymal transition annexin v-fitc/pi staining kras-mutant lung adenocarcinoma renal ischemia/reperfusion injury stimulate eno1-dependent glycolysis lipid-reactive oxygen species epithelial mesenchymal transition cystine deprivation-induced ferroptosis methylated rna immune-precipitation ischemia/reperfusion-related damage [33 small-cell lung cancer kaplan–meier os analysis ferroptosis-mediated tissue injury cancer n6-methyladenosine modification strand-specific library preparation lc-bio bio-tech intestinal ischemia/reperfusion ca2+/cam-dependent pathway cystine/glutamate antiporter xct article download pdf mettl3-mediated m6a modification real-time quantitative pcr hrp-conjugated secondary antibodies specific pathogen-free conditions focad-fak signaling pathway oligo-attached magnetic beads m6a-igf2bp2/3-dependent manner [23] calcium/calmodulin-dependent ferroptosis cell-derived xenografts exhibited cystine transporter slc7a11/xct cancer-related mortalities worldwide significant inhibitory effect mettl3-deficient group grew pancreatic ductal adenocarcinoma full access ap-mn-ms-rna-250 nuclear factor-erythroid 2 enhancing c-myc stability acute myeloid leukemia slc7a11 mrna half-lives oncogenic kras-mutant cancers iron-dependent ros production pex-3-mettl3 expression plasmid rip-qpcr analysis showed rna n6-methyladenosine potential anti-tumor effect privacy choices/manage cookies rna immune-precipitation lung adenocarcinoma mettl3-mediated methylation

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         headline:METTL3 promotes lung adenocarcinoma tumor growth and inhibits ferroptosis by stabilizing SLC7A11 m6A modification
         description:N6-methyladenosine (m6A) has emerged as a significant regulator of the progress of various cancers. However, its role in lung adenocarcinoma (LUAD) remains unclear. Here, we explored the biological function and underlying mechanism of methyltransferase-like 3 (METTL3), the main catalyst of m6A, in LUAD progression. The expression of m6A, METTL3, YTHDF1 and SLC7A11 were detected by immunochemistry or/and online datasets in LUAD patients. The effects of METTL3 on LUAD cell proliferation, apoptosis and ferroptosis were assessed through in vitro loss-and gain-of-function experiments. The in vivo effect on tumorigenesis of METTL3 was evaluated using the LUAD cell xenograft mouse model. MeRIP-seq, RNA immunoprecipitation and RNA stability assay were conducted to explore the molecular mechanism of METTL3 in LUAD. The results showed that the m6A level, as well as the methylase METTL3 were both significantly elevated in LUAD patients and lung cancer cells. Functionally, we found that METTL3 could promote proliferation and inhibit ferroptosis in different LUAD cell models, while METTL3 knockdown suppressed LUAD growth in cell-derived xenografts. Mechanistically, solute carrier 7A11 (SLC7A11), the subunit of system Xc−, was identified as the direct target of METTL3 by mRNA-seq and MeRIP-seq. METTL3-mediated m6A modification could stabilize SLC7A11 mRNA and promote its translation, thus promoting LUAD cell proliferation and inhibiting cell ferroptosis, a novel form of programmed cell death. Additionally, we demonstrated that YTHDF1, a m6A reader, was recruited by METTL3 to enhance SLC7A11 m6A modification. Moreover, the expression of YTHDF1 and SLC7A11 were positively correlated with METTL3 and m6A in LUAD tissues. These findings reinforced the oncogenic role of METTL3 in LUAD progression and revealed its underlying correlation with cancer cell ferroptosis; these findings also indicate that METTL3 is a promising novel target in LUAD diagnosis and therapy.
         datePublished:2022-01-07T00:00:00Z
         dateModified:2022-01-07T00:00:00Z
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            Lung adenocarcinoma
            METTL3
            N6-methyladenosine (m6a) modification
            Ferroptosis
            SLC7A11
            Cancer Research
            Cell Biology
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      headline:METTL3 promotes lung adenocarcinoma tumor growth and inhibits ferroptosis by stabilizing SLC7A11 m6A modification
      description:N6-methyladenosine (m6A) has emerged as a significant regulator of the progress of various cancers. However, its role in lung adenocarcinoma (LUAD) remains unclear. Here, we explored the biological function and underlying mechanism of methyltransferase-like 3 (METTL3), the main catalyst of m6A, in LUAD progression. The expression of m6A, METTL3, YTHDF1 and SLC7A11 were detected by immunochemistry or/and online datasets in LUAD patients. The effects of METTL3 on LUAD cell proliferation, apoptosis and ferroptosis were assessed through in vitro loss-and gain-of-function experiments. The in vivo effect on tumorigenesis of METTL3 was evaluated using the LUAD cell xenograft mouse model. MeRIP-seq, RNA immunoprecipitation and RNA stability assay were conducted to explore the molecular mechanism of METTL3 in LUAD. The results showed that the m6A level, as well as the methylase METTL3 were both significantly elevated in LUAD patients and lung cancer cells. Functionally, we found that METTL3 could promote proliferation and inhibit ferroptosis in different LUAD cell models, while METTL3 knockdown suppressed LUAD growth in cell-derived xenografts. Mechanistically, solute carrier 7A11 (SLC7A11), the subunit of system Xc−, was identified as the direct target of METTL3 by mRNA-seq and MeRIP-seq. METTL3-mediated m6A modification could stabilize SLC7A11 mRNA and promote its translation, thus promoting LUAD cell proliferation and inhibiting cell ferroptosis, a novel form of programmed cell death. Additionally, we demonstrated that YTHDF1, a m6A reader, was recruited by METTL3 to enhance SLC7A11 m6A modification. Moreover, the expression of YTHDF1 and SLC7A11 were positively correlated with METTL3 and m6A in LUAD tissues. These findings reinforced the oncogenic role of METTL3 in LUAD progression and revealed its underlying correlation with cancer cell ferroptosis; these findings also indicate that METTL3 is a promising novel target in LUAD diagnosis and therapy.
      datePublished:2022-01-07T00:00:00Z
      dateModified:2022-01-07T00:00:00Z
      pageStart:1
      pageEnd:16
      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s12935-021-02433-6
      keywords:
         Lung adenocarcinoma
         METTL3
         N6-methyladenosine (m6a) modification
         Ferroptosis
         SLC7A11
         Cancer Research
         Cell Biology
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               type:PostalAddress
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      name:Yangfeng Shi
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            name:Affiliated Hangzhou First People’s Hospital, Zhejiang University School of Medicine
            address:
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      name:Department of Respiratory and Critical Medicine, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China
      name:Cancer Center, Zhejiang University, Hangzhou, China
      name:Department of Respiratory and Critical Medicine, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China
      name:Cancer Center, Zhejiang University, Hangzhou, China
      name:Department of Respiratory and Critical Medicine, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China
      name:Cancer Center, Zhejiang University, Hangzhou, China
      name:Department of Pathology and Pathophysiology, Zhejiang University School of Medicine, Hangzhou, China
      name:Department of Respiratory and Critical Medicine, Affiliated Hangzhou First People’s Hospital, Zhejiang University School of Medicine, Hangzhou, China
      name:Department of Respiratory and Critical Medicine, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China
      name:Cancer Center, Zhejiang University, Hangzhou, China

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