Alternative Splicing in Cancer
A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".
Deadline for manuscript submissions: closed (15 July 2023) | Viewed by 1244
Special Issue Editor
Interests: RNA biology; alternative splicing; splice factors; tumor biology; novel therapeutics
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Approximately 94% of genes are alternatively spliced (AS) in humans, and there are thousands of isoforms specifically associated with disease progression. Splicing variants are described in virtually every class of molecules, from growth factors to tyrosine kinase/phosphatase receptors to tumor suppressors and oncogenes. Frequently, the splicing isoforms have opposing functions, e.g., pro- or anti-angiogenic, pro- or anti-apoptotic. A recent report demonstrates that the function of splice isoforms may be as different as being encoded by distinct genes, underlining the importance of AS in gene regulation and modulation of the cells’ functional repertoire. Unsurprisingly, given its extent, numerous splice isoforms have been described to be associated with cancer, and aberrant splicing is recognized as one of the hallmarks of cancer. Besides the implications for cancer pathogenesis, de-regulated alternative splicing is recognized as one of the novel areas of cell biology where therapeutic manipulations may be designed. Indeed, using either small molecules or splicing-switching oligonucleotides, faulty splice isoforms may be switched back to their normal counterparts and therefore inhibit tumor growth. Aberrant AS is also emerging as a novel mechanism in drug chemoresistance.
This Special Issue welcomes the submission of research papers or reviews on any aspect linking constitutive or alternative splicing to cancer progression, pathologic mechanisms, or therapeutic aspects.
Dr. Sebastian Oltean
Guest Editor
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