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...

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Bibliographic Details
Published in:International journal of molecular sciences 2022-09, Vol.23 (18), p.10918
Main Authors: Kim, Woo Ryung, Park, Eun Gyung, Lee, Yun Ju, Bae, Woo Hyeon, Lee, Du Hyeong, Kim, Heui-Soo
Format: Article
Language:English
Subjects:
Alternative Splicing
Apoptosis
Biological activity
Breast cancer
Cancer
Codon, Terminator
Codons
Disease
DNA Transposable Elements - genetics
Epigenesis, Genetic
Epigenetics
Evolution & development
Gene expression
Genetic diversity
Genomes
Humans
Insertion
Integration
Kinases
Metabolism
MicroRNAs - genetics
miRNA
miRNA derived from TE
Mutation
Neoplasms - genetics
Post-transcription
Proteins
Regulatory sequences
Review
Splicing
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Summary: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.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms231810918