دورية أكاديمية
أعرض في EDS

Loss of feedback regulation between FAM3B and androgen receptor driving prostate cancer progression.

التفاصيل البيبلوغرافية
العنوان: Loss of feedback regulation between FAM3B and androgen receptor driving prostate cancer progression.
المؤلفون: Ma T; Department of Structural and Cellular Biology, Tulane University School of Medicine, Tulane Cancer Center, New Orleans, LA, USA.; Southeast Louisiana Veterans Health Care System, New Orleans, LA, USA., Jin L; Department of Structural and Cellular Biology, Tulane University School of Medicine, Tulane Cancer Center, New Orleans, LA, USA.; Southeast Louisiana Veterans Health Care System, New Orleans, LA, USA., Bai S; Department of Structural and Cellular Biology, Tulane University School of Medicine, Tulane Cancer Center, New Orleans, LA, USA., Liu Z; Department of Structural and Cellular Biology, Tulane University School of Medicine, Tulane Cancer Center, New Orleans, LA, USA., Wang S; Department of Structural and Cellular Biology, Tulane University School of Medicine, Tulane Cancer Center, New Orleans, LA, USA.; Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Urological Department, Peking University Cancer Hospital & Institute, Beijing, China., Shen B; Department of Structural and Cellular Biology, Tulane University School of Medicine, Tulane Cancer Center, New Orleans, LA, USA.; Hubei Key Laboratory of Embryonic Stem Cell Research, Hubei University of Medicine, Shiyan, Hubei, China., Cho Y; Department of Structural and Cellular Biology, Tulane University School of Medicine, Tulane Cancer Center, New Orleans, LA, USA.; Southeast Louisiana Veterans Health Care System, New Orleans, LA, USA., Cao S; Department of Structural and Cellular Biology, Tulane University School of Medicine, Tulane Cancer Center, New Orleans, LA, USA., Sun MJS; Department of Biochemistry and Molecular Biology, Tulane University School of Medicine, New Orleans, LA, USA., Fazli L; Department of Urologic Sciences, Vancouver Prostate Centre, University of British Columbia, Vancouver, BC, Canada., Zhang D; Department of Structural and Cellular Biology, Tulane University School of Medicine, Tulane Cancer Center, New Orleans, LA, USA.; Duke University, Durham, NC, USA., Wedderburn C; Department of Structural and Cellular Biology, Tulane University School of Medicine, Tulane Cancer Center, New Orleans, LA, USA., Zhang DY; Department of Structural and Cellular Biology, Tulane University School of Medicine, Tulane Cancer Center, New Orleans, LA, USA.; University of Southern California, Los Angeles, CA, USA., Mugon G; Department of Biochemistry and Molecular Biology, Tulane University School of Medicine, New Orleans, LA, USA., Ungerleider N; Department of Pathology, Tulane University School of Medicine, Tulane Cancer Center, New Orleans, LA, USA., Baddoo M; Department of Pathology, Tulane University School of Medicine, Tulane Cancer Center, New Orleans, LA, USA., Zhang K; Department of Computer Science, Bioinformatics Facility of Xavier RCMI Center of Cancer Research, Xavier University of Louisiana, New Orleans, LA, USA., Schiavone LH; Discovery Biology, Discovery Sciences, R&D, AstraZeneca, Gothenburg, Sweden., Burkhardt BR; Department of Cell Biology, Microbiology and Molecular Biology, University of South Florida, Tampa, FL, USA., Fan J; Department of Biochemistry and Molecular Biology, Tulane University School of Medicine, New Orleans, LA, USA., You Z; Department of Structural and Cellular Biology, Tulane University School of Medicine, Tulane Cancer Center, New Orleans, LA, USA.; Southeast Louisiana Veterans Health Care System, New Orleans, LA, USA., Flemington EK; Department of Pathology, Tulane University School of Medicine, Tulane Cancer Center, New Orleans, LA, USA., Dong X; Department of Urologic Sciences, Vancouver Prostate Centre, University of British Columbia, Vancouver, BC, Canada., Dong Y; Department of Structural and Cellular Biology, Tulane University School of Medicine, Tulane Cancer Center, New Orleans, LA, USA.; Southeast Louisiana Veterans Health Care System, New Orleans, LA, USA.
المصدر: Journal of the National Cancer Institute [J Natl Cancer Inst] 2024 Mar 07; Vol. 116 (3), pp. 421-433.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Oxford University Press Country of Publication: United States NLM ID: 7503089 Publication Model: Print Cited Medium: Internet ISSN: 1460-2105 (Electronic) Linking ISSN: 00278874 NLM ISO Abbreviation: J Natl Cancer Inst Subsets: MEDLINE
أسماء مطبوعة: Publication: <2003-> : Cary, NC : Oxford University Press
Original Publication: Bethesda, Md., U. S. Dept. of Health, Education, and Welfare, Public Health Service, National Institutes of Health; Washington, for sale by the Supt. of Docs., U. S. Govt. Print. Off.
مواضيع طبية MeSH: Receptors, Androgen*/genetics , Prostatic Neoplasms*/genetics , Prostatic Neoplasms*/metabolism, Male ; Humans ; Feedback ; Transcriptome ; Oncogene Proteins, Fusion/genetics ; Transcriptional Regulator ERG/genetics ; Transcriptional Regulator ERG/metabolism ; Neoplasm Proteins/genetics ; Cytokines/genetics
مستخلص: Background: Although the fusion of the transmembrane serine protease 2 gene (TMPRSS2) with the erythroblast transformation-specific-related gene (ERG), or TMPRSS2-ERG, occurs frequently in prostate cancer, its impact on clinical outcomes remains controversial. Roughly half of TMPRSS2-ERG fusions occur through intrachromosomal deletion of interstitial genes and the remainder via insertional chromosomal rearrangements. Because prostate cancers with deletion-derived TMPRSS2-ERG fusions are more aggressive than those with insertional fusions, we investigated the impact of interstitial gene loss on prostate cancer progression.
Methods: We conducted an unbiased analysis of transcriptome data from large collections of prostate cancer samples and employed diverse in vitro and in vivo models combined with genetic approaches to characterize the interstitial gene loss that imposes the most important impact on clinical outcome.
Results: This analysis identified FAM3B as the top-ranked interstitial gene whose loss is associated with a poor prognosis. The association between FAM3B loss and poor clinical outcome extended to fusion-negative prostate cancers where FAM3B downregulation occurred through epigenetic imprinting. Importantly, FAM3B loss drives disease progression in prostate cancer. FAM3B acts as an intermediator of a self-governing androgen receptor feedback loop. Specifically, androgen receptor upregulates FAM3B expression by binding to an intronic enhancer to induce an enhancer RNA and facilitate enhancer-promoter looping. FAM3B, in turn, attenuates androgen receptor signaling.
Conclusion: Loss of FAM3B in prostate cancer, whether through the TMPRSS2-ERG translocation or epigenetic imprinting, causes an exit from this autoregulatory loop to unleash androgen receptor activity and prostate cancer progression. These findings establish FAM3B loss as a new driver of prostate cancer progression and support the utility of FAM3B loss as a biomarker to better define aggressive prostate cancer.
(© The Author(s) 2023. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com.)
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معلومات مُعتمدة: Canada CAPMC CIHR; #I01 BX00492901 United States VA VA; I01 BX004929 United States BX BLRD VA; U54 MD007595 United States MD NIMHD NIH HHS; P01 CA214091 United States CA NCI NIH HHS; #PTJ156150 United States NH NIH HHS
المشرفين على المادة: 0 (Receptors, Androgen)
0 (Oncogene Proteins, Fusion)
0 (Transcriptional Regulator ERG)
0 (FAM3B protein, human)
0 (Neoplasm Proteins)
0 (Cytokines)
تواريخ الأحداث: Date Created: 20231017 Date Completed: 20240308 Latest Revision: 20240309
رمز التحديث: 20240309
مُعرف محوري في PubMed: PMC10919334
DOI: 10.1093/jnci/djad215
PMID: 37847647
قاعدة البيانات: MEDLINE
الوصف
تدمد:1460-2105
DOI:10.1093/jnci/djad215