دورية أكاديمية
أعرض في EDS

Alternative splicing in prostate cancer progression and therapeutic resistance.

التفاصيل البيبلوغرافية
العنوان: Alternative splicing in prostate cancer progression and therapeutic resistance.
المؤلفون: Rawat C; Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA., Heemers HV; Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA. heemerh@ccf.org.
المصدر: Oncogene [Oncogene] 2024 May; Vol. 43 (22), pp. 1655-1668. Date of Electronic Publication: 2024 Apr 24.
نوع المنشور: Journal Article; Review
اللغة: English
بيانات الدورية: Publisher: Nature Publishing Group Country of Publication: England NLM ID: 8711562 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1476-5594 (Electronic) Linking ISSN: 09509232 NLM ISO Abbreviation: Oncogene Subsets: MEDLINE
أسماء مطبوعة: Publication: <2002->: Basingstoke : Nature Publishing Group
Original Publication: Basingstoke, Hampshire, UK : Scientific & Medical Division, MacMillan Press, c1987-
مواضيع طبية MeSH: Alternative Splicing*/genetics , Drug Resistance, Neoplasm*/genetics , Disease Progression* , Prostatic Neoplasms, Castration-Resistant*/genetics , Prostatic Neoplasms, Castration-Resistant*/pathology , Prostatic Neoplasms, Castration-Resistant*/therapy , Prostatic Neoplasms*/genetics , Prostatic Neoplasms*/pathology , Prostatic Neoplasms*/therapy, Humans ; Male ; Gene Expression Regulation, Neoplastic ; Animals
مستخلص: Prostate cancer (CaP) remains the second leading cause of cancer deaths in western men. CaP mortality results from diverse molecular mechanisms that mediate resistance to the standard of care treatments for metastatic disease. Recently, alternative splicing has been recognized as a hallmark of CaP aggressiveness. Alternative splicing events cause treatment resistance and aggressive CaP behavior and are determinants of the emergence of the two major types of late-stage treatment-resistant CaP, namely castration-resistant CaP (CRPC) and neuroendocrine CaP (NEPC). Here, we review recent multi-omics data that are uncovering the complicated landscape of alternative splicing events during CaP progression and the impact that different gene transcript isoforms can have on CaP cell biology and behavior. We discuss renewed insights in the molecular machinery by which alternative splicing occurs and contributes to the failure of systemic CaP therapies. The potential for alternative splicing events to serve as diagnostic markers and/or therapeutic targets is explored. We conclude by considering current challenges and promises associated with splicing-modulating therapies, and their potential for clinical translation into CaP patient care.
(© 2024. The Author(s).)
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معلومات مُعتمدة: R01 CA248048 United States CA NCI NIH HHS; CA248048 U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI); N/A Republic of Korea National Cancer Center; CA166440 U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)
تواريخ الأحداث: Date Created: 20240424 Date Completed: 20240529 Latest Revision: 20240701
رمز التحديث: 20240702
مُعرف محوري في PubMed: PMC11136669
DOI: 10.1038/s41388-024-03036-x
PMID: 38658776
قاعدة البيانات: MEDLINE
الوصف
تدمد:1476-5594
DOI:10.1038/s41388-024-03036-x