Almost all tumors harbor a defective negative feedback loop of signaling by transforming growth factor-β (TGF-β). Epigenetic mechanisms of gene regulation, including DNA methylation, are fundamental to normal cellular function and also play a major role in carcinogenesis. Recent evidence demonstrated that TGF-β signaling mediates cancer development and progression. Many key events in TGF-β signaling in cancer included auto-induction of TGF-β1 and increased expression of DNA methyltransferases (DNMTs), suggesting that DNA methylation plays a significant role in cancer development and progression. In this review, we performed an extensive survey of the literature linking TGF-β signaling to DNA methylation in prostate cancer. It appeared that almost all DNA methylated genes detected in prostate cancer are directly or indirectly related to TGF-β signaling. This knowledge has provided a basis for our future directions of prostate cancer research and strategies for prevention and therapy for prostate cancer.
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http://dx.doi.org/10.3978/j.issn.2223-4683.2012.05.06 | DOI Listing |
JCO Precis Oncol
January 2025
Medical Research Service, Department of Veterans Affairs, Tennessee Valley Healthcare System, Nashville, TN.
Purpose: Considerable genetic heterogeneity is currently thought to underlie hereditary prostate cancer (HPC). Most families meeting criteria for HPC cannot be attributed to currently known pathogenic variants.
Methods: To discover pathogenic variants predisposing to prostate cancer, we conducted a familial case-control association study using both genome-wide single-allele and identity-by-descent analytic approaches.
Cancer Res Commun
January 2025
University of Minnesota, Minnesota, MN, United States.
Neuroendocrine neoplasms (NENs) encompass a diverse set of malignancies with limited precision therapy options. Recently, therapies targeting DLL3 have shown clinical efficacy in aggressive NENs, including small cell lung cancers and neuroendocrine prostate cancers. Given the continued development and expansion of DLL3-targeted therapies, we sought to characterize the expression of DLL3 and identify its clinical and molecular correlates across diverse neuroendocrine and non-neuroendocrine cancers.
View Article and Find Full Text PDFAsian Pac J Cancer Prev
January 2025
Department of Biotechnology, Kakatiya University, Warangal, Telangana, India.
Objective: A new library of Thiazolidine-2,4-dione-biphenyl Derivatives derivatives (10a-j) was designed and synthesized. All compounds were characterized by spectral data. Further, these were evaluated for their in vitro anticancer activity.
View Article and Find Full Text PDFAsian Pac J Cancer Prev
January 2025
Postgraduate Program in Oncology, Haroldo Juaçaba Hospital, Ceará Cancer Institute (ICC), Brazil.
Objective: This study aimed to investigate the influence of p16 immunohistochemical expression on the biochemical recurrence rate of pT2-pT3 prostate cancer.
Materials And Methods: A total of 488 pT2-pT3 stage prostate adenocarcinomas undergoing radical prostatectomy were included in this study. Following a review of Gleason classification and retrieval of sociodemographic and clinicopathological data, as well as the date of last consultation and biochemical recurrence, immunohistochemistry for p16 was performed.
FASEB J
January 2025
Prostate Cancer/Genitourologic Program, Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Among the known nuclear exportins, CRM1 is the most studied prototype. Dysregulation of CRM1 occurs in many cancers, hence, understanding the role of CRM1 in cancer can help in developing synergistic therapeutics. The study investigates how CRM1 affects prostate cancer growth and survival.
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