Objective: To analyze the biological network regulation and key proteins of gene expression microarray in human normal prostate epithelial cells after treated with low-dose cadmium, and provide some new theoretical evidence for the pathogenesis of cadmium-related prostate cancer.
Methods: We downloaded 19 copies of gene chip data from the Gene Expression Omnibus (GEO), involving 9 samples of prostate epithelial cells exposed to low-dose cadmium and 10 cases of normal control. Using the Gene-Cloud of Biotechnology Informs platform, GenClip2.0 and Sytoscape 3.5.1, we screened differentially expressed genes, explored their protein interaction networks and biological pathways and, from the perspective of transcriptome, analyzed the changes in the genetic network of normal human prostate epithelial cells and their possible molecular biological functions after low-dose cadmium treatment.
Results: Totally, 1 050 (1.92%) differentially expressed genes were found in the prostate epithelial cells treated with low-dose cadmium, involved in such biological functions as the cell physiological process, MAPK regulation, regulation of intracellular signal transduction, and immunological effect. The HSP90AB1, BUB3 and PRKAR1A genes were the core nodes of the protein network, which showed statistically significant differences in their expressions and a correlation with the malignant transformation of normal cells.
Conclusions: Low-dose cadmium can cause genetic changes in normal human prostate epithelial cells and the differentially expressed genes are mainly involved in such biological functions as the cell physiological process, MAPK regulation, regulation of intracellular signal transduction, and immunological effect.
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J Cell Mol Med
January 2025
Department of Andrology, The First Hospital of Jilin University, Changchun, China.
Prostate cancer (PCa) is one of the most common cancers in men worldwide. Autophagy-related genes (ARGs) may play an important role in various biological processes of PCa. The aim of this study was to identify and evaluate autophagy-related features to predict clinical outcomes in patients with PCa.
View Article and Find Full Text PDFKaohsiung J Med Sci
January 2025
Department of Urology, Tianjin First Central Hospital, Tianjin, China.
miR-155 exhibits variable expression in different tumors and fulfills diverse biological roles. However, specific molecular mechanisms by which miR-155-5p, which is under-expressed in prostate cancer (PCa), operates are yet to be elucidated. The role of the enhancer of zeste 2 (EZH2)/miR-155-5p axis in PCa was determined by using bioinformatics tools and performing luciferase reporter assay, chromatin immunoprecipitation PCR, CCK-8 assays, cell migration and invasion assays, RNA isolation, reverse transcription quantity (RT-qPCR) and Western blot.
View Article and Find Full Text PDFBMC Cancer
January 2025
Department of Urology, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Background: Prostate cancer (PCa) is commonly occurred among males worldwide and its prognosis could be influenced by biochemical recurrence (BCR). MicroRNAs (miRNAs) are functional regulators in carcinogenesis, and miR-221-3p was reported as one of the significant candidates deregulated in PCa. However, its regulatory pattern in PCa BCR across literature reports was not consistent, and the targets and mechanisms in PCa malignant transition and BCR are less explored.
View Article and Find Full Text PDFCurr Mol Pharmacol
January 2025
School of Medicine, Yichun University, 576 XueFu Road, Yuanzhou District, Yichun 336000, Jiangxi Province, China.
Background: Finasteride and doxazosin are used for the treatment of benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS). Epithelial-mesenchymal transition (EMT) plays an important role in BPH, little is known about the growth inhibition and anti-fibrosis effects of doxazosin on the regulation of EMT and morphology in the prostate.
Objectives: The present study examined the effects of doxazosin on testosterone propionate (TP)-induced prostate growth in vivo and in vitro and its impact on the EMT and TGF-β/Smad signaling pathway.
bioRxiv
December 2024
Michigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, 48109.
Inadequate response to androgen deprivation therapy (ADT) frequently arises in prostate cancer, driven by cellular mechanisms that remain poorly understood. Here, we integrated single-cell RNA sequencing, single-cell multiomics, and spatial transcriptomics to define the transcriptional, epigenetic, and spatial basis of cell identity and castration response in the mouse prostate. Leveraging these data along with a meta-analysis of human prostates and prostate cancer, we identified cellular orthologs and key determinants of ADT response and resistance.
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