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MYC-regulated pseudogene HMGA1P6 promotes ovarian cancer malignancy via augmenting the oncogenic HMGA1/2
Pseudogenes have long been considered as nonfunctional genomic sequences. Recent studies have shown that they can potentially regulate the expression of protein-coding genes and are dysregulated in diseases including cancer. However, the potential roles of pseudogenes in ovarian cancer have not been...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7054391/ https://www.ncbi.nlm.nih.gov/pubmed/32127525 http://dx.doi.org/10.1038/s41419-020-2356-9 |
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author | Tian, Xiaoxue Song, Jianping Zhang, Xiyu Yan, Mingyao Wang, Shourong Wang, Yuqiong Xu, Limei Zhao, Ling Wei, Jian-jun Shao, Changshun Kong, Beihua Liu, Zhaojian |
author_facet | Tian, Xiaoxue Song, Jianping Zhang, Xiyu Yan, Mingyao Wang, Shourong Wang, Yuqiong Xu, Limei Zhao, Ling Wei, Jian-jun Shao, Changshun Kong, Beihua Liu, Zhaojian |
author_sort | Tian, Xiaoxue |
collection | PubMed |
description | Pseudogenes have long been considered as nonfunctional genomic sequences. Recent studies have shown that they can potentially regulate the expression of protein-coding genes and are dysregulated in diseases including cancer. However, the potential roles of pseudogenes in ovarian cancer have not been well studied. Here we characterized the pseudogene expression profile in HGSOC (high-grade serous ovarian carcinoma) by microarray. We identified 577 dysregulated pseudogenes and most of them were up-regulated (538 of 577). HMGA1P6 (High mobility group AT-hook 1 pseudogene 6) was one of the overexpressed pseudogenes and its expression was inversely correlated with patient survival. Mechanistically, HMGA1P6 promoted ovarian cancer cell malignancy by acting as a ceRNA (competitive endogenous RNA) that led to enhanced HMGA1 and HMGA2 expression. Importantly, HMGA1P6 was transcriptionally activated by oncogene MYC in ovarian cancer. Our findings reveal that MYC may contribute to oncogenesis through transcriptional regulation of pseudogene HMGA1P6 in ovarian cancer. |
format | Online Article Text |
id | pubmed-7054391 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-70543912020-03-05 MYC-regulated pseudogene HMGA1P6 promotes ovarian cancer malignancy via augmenting the oncogenic HMGA1/2 Tian, Xiaoxue Song, Jianping Zhang, Xiyu Yan, Mingyao Wang, Shourong Wang, Yuqiong Xu, Limei Zhao, Ling Wei, Jian-jun Shao, Changshun Kong, Beihua Liu, Zhaojian Cell Death Dis Article Pseudogenes have long been considered as nonfunctional genomic sequences. Recent studies have shown that they can potentially regulate the expression of protein-coding genes and are dysregulated in diseases including cancer. However, the potential roles of pseudogenes in ovarian cancer have not been well studied. Here we characterized the pseudogene expression profile in HGSOC (high-grade serous ovarian carcinoma) by microarray. We identified 577 dysregulated pseudogenes and most of them were up-regulated (538 of 577). HMGA1P6 (High mobility group AT-hook 1 pseudogene 6) was one of the overexpressed pseudogenes and its expression was inversely correlated with patient survival. Mechanistically, HMGA1P6 promoted ovarian cancer cell malignancy by acting as a ceRNA (competitive endogenous RNA) that led to enhanced HMGA1 and HMGA2 expression. Importantly, HMGA1P6 was transcriptionally activated by oncogene MYC in ovarian cancer. Our findings reveal that MYC may contribute to oncogenesis through transcriptional regulation of pseudogene HMGA1P6 in ovarian cancer. Nature Publishing Group UK 2020-03-03 /pmc/articles/PMC7054391/ /pubmed/32127525 http://dx.doi.org/10.1038/s41419-020-2356-9 Text en © The Author(s) 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Tian, Xiaoxue Song, Jianping Zhang, Xiyu Yan, Mingyao Wang, Shourong Wang, Yuqiong Xu, Limei Zhao, Ling Wei, Jian-jun Shao, Changshun Kong, Beihua Liu, Zhaojian MYC-regulated pseudogene HMGA1P6 promotes ovarian cancer malignancy via augmenting the oncogenic HMGA1/2 |
title | MYC-regulated pseudogene HMGA1P6 promotes ovarian cancer malignancy via augmenting the oncogenic HMGA1/2 |
title_full | MYC-regulated pseudogene HMGA1P6 promotes ovarian cancer malignancy via augmenting the oncogenic HMGA1/2 |
title_fullStr | MYC-regulated pseudogene HMGA1P6 promotes ovarian cancer malignancy via augmenting the oncogenic HMGA1/2 |
title_full_unstemmed | MYC-regulated pseudogene HMGA1P6 promotes ovarian cancer malignancy via augmenting the oncogenic HMGA1/2 |
title_short | MYC-regulated pseudogene HMGA1P6 promotes ovarian cancer malignancy via augmenting the oncogenic HMGA1/2 |
title_sort | myc-regulated pseudogene hmga1p6 promotes ovarian cancer malignancy via augmenting the oncogenic hmga1/2 |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7054391/ https://www.ncbi.nlm.nih.gov/pubmed/32127525 http://dx.doi.org/10.1038/s41419-020-2356-9 |
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