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Updated: Jul 8, 2025

Detection of Alternative Splicing During Epithelial-Mesenchymal Transition
Published on: October 9, 2014
RNA-binding proteins regulating the CD44 alternative splicing
Diana Maltseva1, Alexander Tonevitsky1,2
1Faculty of Biology and Biotechnology, HSE University, Moscow, Russia.
Abstract:
Alternative splicing is often deregulated in cancer, and cancer-specific isoform switches are part of the oncogenic transformation of cells. Accumulating evidence indicates that isoforms of the multifunctional cell-surface glycoprotein CD44 play different roles in cancer cells as compared to normal cells. In particular, the shift of CD44 isoforms is required for epithelial to mesenchymal transition (EMT) and is crucial for the maintenance of pluripotency in normal human cells and the acquisition of cancer stem cells phenotype for malignant cells. The growing and seemingly promising use of splicing inhibitors for treating cancer and other pathologies gives hope for the prospect of using such an approach to regulate CD44 alternative splicing. This review integrates current knowledge about regulating CD44 alternative splicing by RNA-binding proteins.
Insights
Alternative splicing of CD44 (a cell surface glycoprotein) is altered in cancer, impacting cell functions. RNA-binding proteins regulate these CD44 splicing changes, offering potential therapeutic targets.
Area of Science:
- Molecular Biology
- Cancer Research
- Cell Biology
Background:
- Alternative splicing dysregulation is a hallmark of cancer.
- CD44 isoforms play critical roles in normal and malignant cells, influencing epithelial to mesenchymal transition (EMT) and cancer stem cell phenotypes.
- CD44 isoform switching is vital for pluripotency in normal cells and malignant transformation.
Purpose of the Study:
- To review the regulation of CD44 alternative splicing by RNA-binding proteins.
- To highlight the significance of CD44 isoforms in cancer progression.
- To explore the therapeutic potential of targeting CD44 splicing.
Main Methods:
- Literature review of studies on CD44 alternative splicing.
- Analysis of RNA-binding protein interactions with CD44 pre-mRNA.
- Integration of data on CD44 function in cancer and normal cells.
Main Results:
- Specific RNA-binding proteins modulate CD44 alternative splicing.
- CD44 isoform expression is altered during EMT and in cancer stem cells.
- Dysregulated CD44 splicing contributes to oncogenesis.
Conclusions:
- RNA-binding proteins are key regulators of CD44 alternative splicing.
- Targeting CD44 splicing represents a promising therapeutic strategy for cancer.
- Understanding CD44 splicing regulation is crucial for developing novel cancer treatments.
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