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METTL14 suppresses cancer stem cell phenotype of colorectal cancer via regulating of β-catenin/NANOG

Cancer stem cell (CSC) characteristic contributes to tumor malignancy and progression. The role of N6-methyladenosine (m6A) modification in CSC characteristic is largely unknown. In this study, we found that m6A methyltransferase METTL14 was downregulated in colorectal cancer (CRC) and negatively co...

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Autores principales: Sun, Chun-Lei, Chen, Jiong, Xing, Zhi-Wei, Tao, Gong-Shai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10240663/
https://www.ncbi.nlm.nih.gov/pubmed/37283789
http://dx.doi.org/10.7150/jca.82158
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author Sun, Chun-Lei
Chen, Jiong
Xing, Zhi-Wei
Tao, Gong-Shai
author_facet Sun, Chun-Lei
Chen, Jiong
Xing, Zhi-Wei
Tao, Gong-Shai
author_sort Sun, Chun-Lei
collection PubMed
description Cancer stem cell (CSC) characteristic contributes to tumor malignancy and progression. The role of N6-methyladenosine (m6A) modification in CSC characteristic is largely unknown. In this study, we found that m6A methyltransferase METTL14 was downregulated in colorectal cancer (CRC) and negatively correlated with the poor prognosis of CRC patients. Overexpression of METTL14 inhibited CSC characteristic, while knockdown of METTL14 promoted this characteristic. Through screening, NANOG was identified as the downstream of METTL14. Mechanically, we demonstrated that METTL14 inhibited cancer stem cell characteristic by regulating β-catenin. Collectively, our findings suggested that METTL16/β-catenin /NANOG axis might be promising therapeutic targets for CRC.
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spelling pubmed-102406632023-06-06 METTL14 suppresses cancer stem cell phenotype of colorectal cancer via regulating of β-catenin/NANOG Sun, Chun-Lei Chen, Jiong Xing, Zhi-Wei Tao, Gong-Shai J Cancer Research Paper Cancer stem cell (CSC) characteristic contributes to tumor malignancy and progression. The role of N6-methyladenosine (m6A) modification in CSC characteristic is largely unknown. In this study, we found that m6A methyltransferase METTL14 was downregulated in colorectal cancer (CRC) and negatively correlated with the poor prognosis of CRC patients. Overexpression of METTL14 inhibited CSC characteristic, while knockdown of METTL14 promoted this characteristic. Through screening, NANOG was identified as the downstream of METTL14. Mechanically, we demonstrated that METTL14 inhibited cancer stem cell characteristic by regulating β-catenin. Collectively, our findings suggested that METTL16/β-catenin /NANOG axis might be promising therapeutic targets for CRC. Ivyspring International Publisher 2023-05-15 /pmc/articles/PMC10240663/ /pubmed/37283789 http://dx.doi.org/10.7150/jca.82158 Text en © The author(s) https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.
spellingShingle Research Paper
Sun, Chun-Lei
Chen, Jiong
Xing, Zhi-Wei
Tao, Gong-Shai
METTL14 suppresses cancer stem cell phenotype of colorectal cancer via regulating of β-catenin/NANOG
title METTL14 suppresses cancer stem cell phenotype of colorectal cancer via regulating of β-catenin/NANOG
title_full METTL14 suppresses cancer stem cell phenotype of colorectal cancer via regulating of β-catenin/NANOG
title_fullStr METTL14 suppresses cancer stem cell phenotype of colorectal cancer via regulating of β-catenin/NANOG
title_full_unstemmed METTL14 suppresses cancer stem cell phenotype of colorectal cancer via regulating of β-catenin/NANOG
title_short METTL14 suppresses cancer stem cell phenotype of colorectal cancer via regulating of β-catenin/NANOG
title_sort mettl14 suppresses cancer stem cell phenotype of colorectal cancer via regulating of β-catenin/nanog
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10240663/
https://www.ncbi.nlm.nih.gov/pubmed/37283789
http://dx.doi.org/10.7150/jca.82158
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