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Updated: Jan 14, 2026

Detection of Alternative Splicing During Epithelial-Mesenchymal Transition
Published on: October 9, 2014
Isoform switching in the CD44/ESRP1 axis as a driver of EMT and cancer stemness across tumor types
K Jankowska1, W Wójtowicz1, M Wierzbinka1
1Department of Molecular Biology, Medical University of Silesia, Katowice, Poland; Students Scientific Society, Medical University of Silesia, Katowice, Poland.
Abstract:
Alternative splicing of cluster of differentiation 44 (CD44), regulated by epithelial splicing regulatory protein 1 (ESRP1), plays a critical role in cancer progression. The switch between CD44 variant (CD44v) and standard (CD44s) isoforms is tightly linked to epithelial-mesenchymal transition (EMT), metastatic potential and cancer stem cell (CSC) maintenance. This review integrates recent isoform-resolved findings to elucidate the molecular mechanisms underlying CD44/ESRP1-mediated splicing and its involvement in oncogenic signaling pathways promoting invasion, plasticity and therapy resistance. We also examine cancer-specific CD44 isoform expression patterns and assess their prognostic and therapeutic relevance. We propose that isoform-specific profiling of the CD44/ESRP1 axis may serve as a predictive framework for metastasis and therapy response, paving the way for targeted splicing-based therapeutics.
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