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ALKBH5 regulates IGF1R expression to promote the Proliferation and Tumorigenicity of Endometrial Cancer

N6-methyladenosine (m(6)A) messenger RNA methylation play important role in cell proliferation and tumorigenicity of endometrial cancer, but the key mechanism is not fully clear. Here, we found that RNA demethylase ALKBH5 expression was significantly upregulated in endometrial cancer, ALKBH5 was the...

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Autores principales: Pu, Xiaowen, Gu, Zhuowei, Gu, Zhengrong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7477457/
https://www.ncbi.nlm.nih.gov/pubmed/32913456
http://dx.doi.org/10.7150/jca.46097
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author Pu, Xiaowen
Gu, Zhuowei
Gu, Zhengrong
author_facet Pu, Xiaowen
Gu, Zhuowei
Gu, Zhengrong
author_sort Pu, Xiaowen
collection PubMed
description N6-methyladenosine (m(6)A) messenger RNA methylation play important role in cell proliferation and tumorigenicity of endometrial cancer, but the key mechanism is not fully clear. Here, we found that RNA demethylase ALKBH5 expression was significantly upregulated in endometrial cancer, ALKBH5 was then identified to positively regulate proliferation and invasion of endometrial cancer. Mechanistically, the m(6)A eraser ALKBH5 demethylated target transcripts IGF1R and enhanced IGF1R mRNA stability, consequently promoting IGF1R translation and activating IGF1R signaling pathway. Thus, we demonstrated that ALKBH5 promoted proliferation and invasion of endometrial cancer via erasing IGF1R m(6)A-modifications, which suggests a potential therapeutic target for endometrial cancer.
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spelling pubmed-74774572020-09-09 ALKBH5 regulates IGF1R expression to promote the Proliferation and Tumorigenicity of Endometrial Cancer Pu, Xiaowen Gu, Zhuowei Gu, Zhengrong J Cancer Research Paper N6-methyladenosine (m(6)A) messenger RNA methylation play important role in cell proliferation and tumorigenicity of endometrial cancer, but the key mechanism is not fully clear. Here, we found that RNA demethylase ALKBH5 expression was significantly upregulated in endometrial cancer, ALKBH5 was then identified to positively regulate proliferation and invasion of endometrial cancer. Mechanistically, the m(6)A eraser ALKBH5 demethylated target transcripts IGF1R and enhanced IGF1R mRNA stability, consequently promoting IGF1R translation and activating IGF1R signaling pathway. Thus, we demonstrated that ALKBH5 promoted proliferation and invasion of endometrial cancer via erasing IGF1R m(6)A-modifications, which suggests a potential therapeutic target for endometrial cancer. Ivyspring International Publisher 2020-07-25 /pmc/articles/PMC7477457/ /pubmed/32913456 http://dx.doi.org/10.7150/jca.46097 Text en © The author(s) 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
Pu, Xiaowen
Gu, Zhuowei
Gu, Zhengrong
ALKBH5 regulates IGF1R expression to promote the Proliferation and Tumorigenicity of Endometrial Cancer
title ALKBH5 regulates IGF1R expression to promote the Proliferation and Tumorigenicity of Endometrial Cancer
title_full ALKBH5 regulates IGF1R expression to promote the Proliferation and Tumorigenicity of Endometrial Cancer
title_fullStr ALKBH5 regulates IGF1R expression to promote the Proliferation and Tumorigenicity of Endometrial Cancer
title_full_unstemmed ALKBH5 regulates IGF1R expression to promote the Proliferation and Tumorigenicity of Endometrial Cancer
title_short ALKBH5 regulates IGF1R expression to promote the Proliferation and Tumorigenicity of Endometrial Cancer
title_sort alkbh5 regulates igf1r expression to promote the proliferation and tumorigenicity of endometrial cancer
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7477457/
https://www.ncbi.nlm.nih.gov/pubmed/32913456
http://dx.doi.org/10.7150/jca.46097
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