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Integration of TE Induces Cancer Specific Alternative Splicing Events
Alternative splicing of messenger RNA (mRNA) precursors contributes to genetic diversity by generating structurally and functionally distinct transcripts. In a disease state, alternative splicing promotes incidence and development of several cancer types through regulation of cancer-related biologic...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9502224/ https://www.ncbi.nlm.nih.gov/pubmed/36142830 http://dx.doi.org/10.3390/ijms231810918 |
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author | Kim, Woo Ryung Park, Eun Gyung Lee, Yun Ju Bae, Woo Hyeon Lee, Du Hyeong Kim, Heui-Soo |
author_facet | Kim, Woo Ryung Park, Eun Gyung Lee, Yun Ju Bae, Woo Hyeon Lee, Du Hyeong Kim, Heui-Soo |
author_sort | Kim, Woo Ryung |
collection | PubMed |
description | Alternative splicing of messenger RNA (mRNA) precursors contributes to genetic diversity by generating structurally and functionally distinct transcripts. In a disease state, alternative splicing promotes incidence and development of several cancer types through regulation of cancer-related biological processes. Transposable elements (TEs), having the genetic ability to jump to other regions of the genome, can bring about alternative splicing events in cancer. TEs can integrate into the genome, mostly in the intronic regions, and induce cancer-specific alternative splicing by adjusting various mechanisms, such as exonization, providing splicing donor/acceptor sites, alternative regulatory sequences or stop codons, and driving exon disruption or epigenetic regulation. Moreover, TEs can produce microRNAs (miRNAs) that control the proportion of transcripts by repressing translation or stimulating the degradation of transcripts at the post-transcriptional level. Notably, TE insertion creates a cancer-friendly environment by controlling the overall process of gene expression before and after transcription in cancer cells. This review emphasizes the correlative interaction between alternative splicing by TE integration and cancer-associated biological processes, suggesting a macroscopic mechanism controlling alternative splicing by TE insertion in cancer. |
format | Online Article Text |
id | pubmed-9502224 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-95022242022-09-24 Integration of TE Induces Cancer Specific Alternative Splicing Events Kim, Woo Ryung Park, Eun Gyung Lee, Yun Ju Bae, Woo Hyeon Lee, Du Hyeong Kim, Heui-Soo Int J Mol Sci Review Alternative splicing of messenger RNA (mRNA) precursors contributes to genetic diversity by generating structurally and functionally distinct transcripts. In a disease state, alternative splicing promotes incidence and development of several cancer types through regulation of cancer-related biological processes. Transposable elements (TEs), having the genetic ability to jump to other regions of the genome, can bring about alternative splicing events in cancer. TEs can integrate into the genome, mostly in the intronic regions, and induce cancer-specific alternative splicing by adjusting various mechanisms, such as exonization, providing splicing donor/acceptor sites, alternative regulatory sequences or stop codons, and driving exon disruption or epigenetic regulation. Moreover, TEs can produce microRNAs (miRNAs) that control the proportion of transcripts by repressing translation or stimulating the degradation of transcripts at the post-transcriptional level. Notably, TE insertion creates a cancer-friendly environment by controlling the overall process of gene expression before and after transcription in cancer cells. This review emphasizes the correlative interaction between alternative splicing by TE integration and cancer-associated biological processes, suggesting a macroscopic mechanism controlling alternative splicing by TE insertion in cancer. MDPI 2022-09-18 /pmc/articles/PMC9502224/ /pubmed/36142830 http://dx.doi.org/10.3390/ijms231810918 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Kim, Woo Ryung Park, Eun Gyung Lee, Yun Ju Bae, Woo Hyeon Lee, Du Hyeong Kim, Heui-Soo Integration of TE Induces Cancer Specific Alternative Splicing Events |
title | Integration of TE Induces Cancer Specific Alternative Splicing Events |
title_full | Integration of TE Induces Cancer Specific Alternative Splicing Events |
title_fullStr | Integration of TE Induces Cancer Specific Alternative Splicing Events |
title_full_unstemmed | Integration of TE Induces Cancer Specific Alternative Splicing Events |
title_short | Integration of TE Induces Cancer Specific Alternative Splicing Events |
title_sort | integration of te induces cancer specific alternative splicing events |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9502224/ https://www.ncbi.nlm.nih.gov/pubmed/36142830 http://dx.doi.org/10.3390/ijms231810918 |
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