دورية أكاديمية
أعرض في EDS

Epithelial-Mesenchymal Transition Signaling and Prostate Cancer Stem Cells: Emerging Biomarkers and Opportunities for Precision Therapeutics.

التفاصيل البيبلوغرافية
العنوان: Epithelial-Mesenchymal Transition Signaling and Prostate Cancer Stem Cells: Emerging Biomarkers and Opportunities for Precision Therapeutics.
المؤلفون: Chaves LP; Department of Genetics, Medicine School of Ribeirão Preto, University of São Paulo, Ribeirão Preto 14048-900, SP, Brazil., Melo CM; Department of Genetics, Medicine School of Ribeirão Preto, University of São Paulo, Ribeirão Preto 14048-900, SP, Brazil., Saggioro FP; Pathology Department, Medicine School of Ribeirão Preto, University of São Paulo, Ribeirão Preto 14048-900, SP, Brazil., Reis RBD; Division of Urology, Department of Surgery and Anatomy, Medicine School of Ribeirão Preto, University of São Paulo, Ribeirão Preto 14048-900, SP, Brazil., Squire JA; Department of Genetics, Medicine School of Ribeirão Preto, University of São Paulo, Ribeirão Preto 14048-900, SP, Brazil.; Department of Pathology and Molecular Medicine, Queen's University, Kingston, ON K7L 3N6, Canada.
المصدر: Genes [Genes (Basel)] 2021 Nov 27; Vol. 12 (12). Date of Electronic Publication: 2021 Nov 27.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't; Review
اللغة: English
بيانات الدورية: Publisher: MDPI Country of Publication: Switzerland NLM ID: 101551097 Publication Model: Electronic Cited Medium: Internet ISSN: 2073-4425 (Electronic) Linking ISSN: 20734425 NLM ISO Abbreviation: Genes (Basel) Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Basel : MDPI
مواضيع طبية MeSH: Biomarkers, Tumor/*genetics , Epithelial-Mesenchymal Transition/*genetics , Neoplastic Stem Cells/*metabolism , Prostatic Neoplasms, Castration-Resistant/*genetics , Prostatic Neoplasms, Castration-Resistant/*metabolism , Signal Transduction/*genetics, Animals ; Humans ; Male ; Precision Medicine/methods
مستخلص: Prostate cancers may reactivate a latent embryonic program called the epithelial-mesenchymal transition (EMT) during the development of metastatic disease. Through EMT, tumors can develop a mesenchymal phenotype similar to cancer stem cell traits that contributes to metastasis and variation in therapeutic responses. Some of the recurrent somatic mutations of prostate cancer affect EMT driver genes and effector transcription factors that induce the chromatin- and androgen-dependent epigenetic alterations that characterize castrate-resistant prostate cancer (CRPC). EMT regulators in prostate cancer comprise transcription factors ( SNAI1/2 , ZEB1 , TWIST1 , and ETS), tumor suppressor genes ( RB1 , PTEN , and TP53 ), and post-transcriptional regulators (miRNAs) that under the selective pressures of antiandrogen therapy can develop an androgen-independent metastatic phenotype. In prostate cancer mouse models of EMT, Slug expression, as well as WNT/β-Catenin and notch signaling pathways, have been shown to increase stemness potential. Recent single-cell transcriptomic studies also suggest that the stemness phenotype of advanced prostate cancer may be related to EMT. Other evidence correlates EMT and stemness with immune evasion, for example, activation of the polycomb repressor complex I, promoting EMT and stemness and cytokine secretion through RB1 , TP53 , and PRC1 . These findings are helping clinical trials in CRPC that seek to understand how drugs and biomarkers related to the acquisition of EMT can improve drug response.
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فهرسة مساهمة: Keywords: castrate-resistant prostate cancer; chromatin modification; epigenomics; immune evasion; immunotherapy; mouse models of cancer; oncogenes; plasticity; tumor microenvironment; tumor suppressor genes
المشرفين على المادة: 0 (Biomarkers, Tumor)
تواريخ الأحداث: Date Created: 20211224 Date Completed: 20220223 Latest Revision: 20230921
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC8701270
DOI: 10.3390/genes12121900
PMID: 34946849
قاعدة البيانات: MEDLINE
الوصف
تدمد:2073-4425
DOI:10.3390/genes12121900