We are analyzing https://link.springer.com/article/10.1186/s12935-024-03250-3.

Title:
METTL14 enhances the m6A modification level of lncRNA MSTRG.292666.16 to promote the progression of non-small cell lung cancer | Cancer Cell International
Description:
Background m6A modification has close connection with the occurrence, development, and prognosis of tumors. This study aimed to explore the roles of m6A modification and its related mechanisms in non-small cell lung cancer (NSCLC). Methods NSCLC tissues and their corresponding para-cancerous tissues were collected to determine the m6A levels of total RNA/lncRNAs and the expression of m6A modification-related genes/lncRNAs. Then, A549 cells were transfected with si-METTL14 or oe-METTL14, and the cell transfection efficiency was assessed. Subsequently, the viability, apoptosis, cell colony formation, migration and invasion of the different cells were determined. Finally, the nude mouse tumorigenicity experiments were performed to observe the effects of METTL14 in vivo. Results Compared to the para-NSCLC tissues, the m6A level and METTL14 expression were both significantly increased in the NSCLC tissues (P < 0.05). Based on the expression of METTL14 in the different cell lines, A549 cells were chosen for further experiments. Then, the A549 cells with METTL14 knockdown and overexpression were successfully established, as well as it was found that METTL14 knockdown could inhibit the viability, colony formation, migration, and invasion of A549 cells, while facilitate their apoptosis. In vivo experiments also showed that METTL14 knockdown could inhibit tumor formation and growth. Additionally, the m6A level of MSTRG.292666.16 was higher in the NSCLC tissues; and after METTL14 knockdown, the expression and m6A level of MSTRG.292666.16 were both significantly reduced in A549 cells, and vice versa. Conclusion METTL14 may promote the progression of NSCLC through up-regulating MSTRG.292666.16 and enhance its m6A modification level.
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Keywords {🔍}

cells, mettl, cell, cancer, nsclc, expression, pubmed, article, mstrg, modification, tissues, google, scholar, rna, level, lung, methylation, cas, compared, tumor, fig, lncrna, metastasis, significantly, levels, min, invasion, simettl, shanghai, samples, central, nonsmall, migration, control, apoptosis, formation, effects, knockdown, growth, tissue, total, transfection, found, chen, progression, development, study, viability, mrna, lncrnas,

Topics {✒️}

regulating mir-30c-2-3p/akt1s1 axis mir-374b-5p/srsf7 axis itga11/mir–516b–5p axis regulating mir-30c-2-3p/akt1s1 [28] pi3k/akt/mtor signaling pathway regulating pri-mir-93-5p maturation 16-mir-6836-5p-mapk8ip3 axis [35] 16-mir-6836-5p-mapk8ip3 axis exosomal mir-146a-5p malat/mir-384/mal2 axis a-induced lncdbet promotes small-cell lung cancer article download pdf mettl14-mediated n6-methyladenosine modification fabp5-mediated lipid metabolism lnc-lsg1 m6a modification-related genes/lncrnas drug-resistant lung cancer triple-negative breast cancer lack protein-coding capabilities specific m6a-hypoxia signature guangzhou jet bio-filtration lncrna-mediated posttranslational modifications m6a-hypoxia prognostic signature real-time quantitative pcr main m6a-related enzyme mettl14-mediated m6a modification m6a modification-related genes single targeted therapy lncrnas play cancer-promoting m6a modification patterns lung cancer stem si-nc/ oe-nc 8-μm pore size osimertinib-resistant plasma compared privacy choices/manage cookies boxiong xie revised para-nsclc tissue samples full access human gastric cancer bca assay kit ecl assay kit beas-2b cells m6a-modified lncrnas mstrg including nci-h1650 cells lung cancer cells cell counting kit-8 para-carcinoma tissues tumor suppressor gene regulates gene expression

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WebPage:
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         headline:METTL14 enhances the m6A modification level of lncRNA MSTRG.292666.16 to promote the progression of non-small cell lung cancer
         description:m6A modification has close connection with the occurrence, development, and prognosis of tumors. This study aimed to explore the roles of m6A modification and its related mechanisms in non-small cell lung cancer (NSCLC). NSCLC tissues and their corresponding para-cancerous tissues were collected to determine the m6A levels of total RNA/lncRNAs and the expression of m6A modification-related genes/lncRNAs. Then, A549 cells were transfected with si-METTL14 or oe-METTL14, and the cell transfection efficiency was assessed. Subsequently, the viability, apoptosis, cell colony formation, migration and invasion of the different cells were determined. Finally, the nude mouse tumorigenicity experiments were performed to observe the effects of METTL14 in vivo. Compared to the para-NSCLC tissues, the m6A level and METTL14 expression were both significantly increased in the NSCLC tissues (P < 0.05). Based on the expression of METTL14 in the different cell lines, A549 cells were chosen for further experiments. Then, the A549 cells with METTL14 knockdown and overexpression were successfully established, as well as it was found that METTL14 knockdown could inhibit the viability, colony formation, migration, and invasion of A549 cells, while facilitate their apoptosis. In vivo experiments also showed that METTL14 knockdown could inhibit tumor formation and growth. Additionally, the m6A level of MSTRG.292666.16 was higher in the NSCLC tissues; and after METTL14 knockdown, the expression and m6A level of MSTRG.292666.16 were both significantly reduced in A549 cells, and vice versa. METTL14 may promote the progression of NSCLC through up-regulating MSTRG.292666.16 and enhance its m6A modification level.
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            Cancer Research
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      description:m6A modification has close connection with the occurrence, development, and prognosis of tumors. This study aimed to explore the roles of m6A modification and its related mechanisms in non-small cell lung cancer (NSCLC). NSCLC tissues and their corresponding para-cancerous tissues were collected to determine the m6A levels of total RNA/lncRNAs and the expression of m6A modification-related genes/lncRNAs. Then, A549 cells were transfected with si-METTL14 or oe-METTL14, and the cell transfection efficiency was assessed. Subsequently, the viability, apoptosis, cell colony formation, migration and invasion of the different cells were determined. Finally, the nude mouse tumorigenicity experiments were performed to observe the effects of METTL14 in vivo. Compared to the para-NSCLC tissues, the m6A level and METTL14 expression were both significantly increased in the NSCLC tissues (P < 0.05). Based on the expression of METTL14 in the different cell lines, A549 cells were chosen for further experiments. Then, the A549 cells with METTL14 knockdown and overexpression were successfully established, as well as it was found that METTL14 knockdown could inhibit the viability, colony formation, migration, and invasion of A549 cells, while facilitate their apoptosis. In vivo experiments also showed that METTL14 knockdown could inhibit tumor formation and growth. Additionally, the m6A level of MSTRG.292666.16 was higher in the NSCLC tissues; and after METTL14 knockdown, the expression and m6A level of MSTRG.292666.16 were both significantly reduced in A549 cells, and vice versa. METTL14 may promote the progression of NSCLC through up-regulating MSTRG.292666.16 and enhance its m6A modification level.
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      name:Department of Oncology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China
      name:Department of Oncology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China
      name:Department of Oncology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China
      name:Department of Thoracic, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China
      name:Department of Oncology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China

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