METTL3 promotes non-small cell lung cancer (NSCLC) cell proliferation and colony formation in a m6A-YTHDF1 dependent way
© 2022. The Author(s)..
BACKGROUND: N6-methyladenosine (m6A) is the most common RNA modification, which plays a pivotal role in tumor development and progression. In this study, we assessed the role of m6A methyltransferase METTL3 in FRAS1-involved cell proliferation and colony formation of non-small cell lung cancer (NSCLC) cell lines.
METHODS: Cell viability was analyzed by Cell Counting Kit (CCK-8) and colony formation. M6A RNA immunoprecipitation (IP), Ribosomal immunoprecipitation, RNA immunoprecipitation (RIP) were performed to verify the relationship between METTL3, FRAS1 and YTHDF1. Rescue experiments to confirm the regulatory mechanism of METTL3-FRAS1 promoted NSCLC cell proliferation through CDON by cooperating YTHDF1.
RESULTS: We found that FRAS1 was correlated with poor prognosis in NSCLC patients, of which the transcript undergoes m6A modification regulated by METTL3. METTL3 silence reduced cell viability of NSCLC cells HCC827 and NCI-H1975, which could be restored by FRAS1 overexpression. The m6A modification of FRAS1 could be recognized by YTHDF1. FRAS1 silence or YTHDF1 silence could rescue the elevated NSCLC cell proliferation, colony formation, and tumor growth induced by METTL3 overexpression in vitro and in vivo.
CONCLUSIONS: Our study reveals that METTL3-FRAS1 plays a crucial role in NSCLC cell proliferation, colony formation, and tumor growth through the regulation of CDON by cooperating YTHDF1.
| Errataetall: |
ErratumIn: BMC Pulm Med. 2022 Nov 28;22(1):450. - PMID 36443689 |
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| Medienart: |
E-Artikel |
| Erscheinungsjahr: |
2022 |
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| Erschienen: |
2022 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:22 |
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| Enthalten in: |
BMC pulmonary medicine - 22(2022), 1 vom: 25. Aug., Seite 324 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Dou, Xuejun [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 29.08.2022 Date Revised 28.11.2022 published: Electronic ErratumIn: BMC Pulm Med. 2022 Nov 28;22(1):450. - PMID 36443689 Citation Status MEDLINE |
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| doi: |
10.1186/s12890-022-02119-3 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| 100 | 1 | |a Dou, Xuejun |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a METTL3 promotes non-small cell lung cancer (NSCLC) cell proliferation and colony formation in a m6A-YTHDF1 dependent way |
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| 500 | |a Date Revised 28.11.2022 | ||
| 500 | |a published: Electronic | ||
| 500 | |a ErratumIn: BMC Pulm Med. 2022 Nov 28;22(1):450. - PMID 36443689 | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a © 2022. The Author(s). | ||
| 520 | |a BACKGROUND: N6-methyladenosine (m6A) is the most common RNA modification, which plays a pivotal role in tumor development and progression. In this study, we assessed the role of m6A methyltransferase METTL3 in FRAS1-involved cell proliferation and colony formation of non-small cell lung cancer (NSCLC) cell lines | ||
| 520 | |a METHODS: Cell viability was analyzed by Cell Counting Kit (CCK-8) and colony formation. M6A RNA immunoprecipitation (IP), Ribosomal immunoprecipitation, RNA immunoprecipitation (RIP) were performed to verify the relationship between METTL3, FRAS1 and YTHDF1. Rescue experiments to confirm the regulatory mechanism of METTL3-FRAS1 promoted NSCLC cell proliferation through CDON by cooperating YTHDF1 | ||
| 520 | |a RESULTS: We found that FRAS1 was correlated with poor prognosis in NSCLC patients, of which the transcript undergoes m6A modification regulated by METTL3. METTL3 silence reduced cell viability of NSCLC cells HCC827 and NCI-H1975, which could be restored by FRAS1 overexpression. The m6A modification of FRAS1 could be recognized by YTHDF1. FRAS1 silence or YTHDF1 silence could rescue the elevated NSCLC cell proliferation, colony formation, and tumor growth induced by METTL3 overexpression in vitro and in vivo | ||
| 520 | |a CONCLUSIONS: Our study reveals that METTL3-FRAS1 plays a crucial role in NSCLC cell proliferation, colony formation, and tumor growth through the regulation of CDON by cooperating YTHDF1 | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a CDON | |
| 650 | 4 | |a Cell proliferation | |
| 650 | 4 | |a Colony formation | |
| 650 | 4 | |a FRAS1 | |
| 650 | 4 | |a METTL3 | |
| 650 | 4 | |a Non-small cell lung cancer (NSCLC) | |
| 650 | 4 | |a YTHDF1 | |
| 650 | 7 | |a RNA, Messenger |2 NLM | |
| 650 | 7 | |a RNA-Binding Proteins |2 NLM | |
| 650 | 7 | |a YTHDF1 protein, human |2 NLM | |
| 650 | 7 | |a Methyltransferases |2 NLM | |
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| 650 | 7 | |a METTL3 protein, human |2 NLM | |
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| 700 | 1 | |a Wang, Zhiyuan |e verfasserin |4 aut | |
| 700 | 1 | |a Lu, Weiqiang |e verfasserin |4 aut | |
| 700 | 1 | |a Miao, Libin |e verfasserin |4 aut | |
| 700 | 1 | |a Zhao, Yuefeng |e verfasserin |4 aut | |
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