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This review article examines the critical role of dysregulated RNA splicing in the development and progression of cancer. It explains that alterations in splicing, caused by mutations or changes in splicing factor expression, are a molecular characteristic of nearly all tumor types, promoting behaviors like increased proliferation, metastasis, and resistance to therapy. The text details the basic biology of the spliceosome and discusses how recurrent mutations in factors like SF3B1, SRSF2, U2AF1, and ZRSR2 drive leukemogenesis and other malignancies. Finally, the article provides a comprehensive overview of existing and emerging therapeutic strategies aimed at modulating or inhibiting RNA splicing, including both broad-spectrum spliceosome inhibitors and targeted approaches like antisense oligonucleotides (ASOs) and CRISPR-based tools.
References:
By 淼淼ElvaThis review article examines the critical role of dysregulated RNA splicing in the development and progression of cancer. It explains that alterations in splicing, caused by mutations or changes in splicing factor expression, are a molecular characteristic of nearly all tumor types, promoting behaviors like increased proliferation, metastasis, and resistance to therapy. The text details the basic biology of the spliceosome and discusses how recurrent mutations in factors like SF3B1, SRSF2, U2AF1, and ZRSR2 drive leukemogenesis and other malignancies. Finally, the article provides a comprehensive overview of existing and emerging therapeutic strategies aimed at modulating or inhibiting RNA splicing, including both broad-spectrum spliceosome inhibitors and targeted approaches like antisense oligonucleotides (ASOs) and CRISPR-based tools.
References: