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Updated: Sep 17, 2025

Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells
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Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells

Published on: April 26, 2017

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Best evidence linking the extracellular factor TGF-β to cancer-associated alternative splicing programs

Opeoluwa Alli-Oke1, Jean-Philippe Brosseau1,2,3

  • 1Department of Biochemistry and Functional Genomic, Sherbrooke, QC, J1E4K8, Canada.

BBA Advances
|June 30, 2025
PubMed

Insights

Transforming growth factor beta 1 (TGF-β) may regulate cancer-associated alternative splicing. This extracellular factor influences cell phenotypes, potentially driving splicing programs critical for cancer progression.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • RNA Biology

Background:

  • Alternative splicing generates diverse RNA transcripts from a single gene.
  • Splicing factors, RNA-binding proteins, control splicing decisions.
  • Regulation of splicing factors and alternative splicing by extracellular factors is understudied.

Purpose of the Study:

  • To investigate the role of extracellular factors in regulating alternative splicing.
  • To explore the potential of transforming growth factor beta 1 (TGF-β) in driving cancer-associated alternative splicing programs.

Main Methods:

  • Review of existing literature on splicing factors and TGF-β.
  • Analysis of known examples linking alternative splicing variants or splicing factors to cancer hallmarks.
  • Correlation of TGF-β's known cellular effects with alternative splicing regulation.

Main Results:

  • TGF-β is a known regulator of multiple cancer-associated cell phenotypes.
  • Alternative splicing variants and their regulatory factors are implicated in cancer hallmarks.
  • Evidence suggests a link between TGF-β signaling and cancer-associated alternative splicing.

Conclusions:

  • TGF-β signaling may play a significant role in orchestrating alternative splicing programs in cancer.
  • Further research is warranted to elucidate the mechanisms by which TGF-β influences alternative splicing in cancer.
Keywords:
Alternative splicingCancerTGFb

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