Exploring the molecular interface of gene expression dynamics and prostate cancer susceptibility in response to HBCD exposure.

Toxicol Res (Camb)

Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, No. 100, Cross Street, Hongshan Road, Jiangsu Province, Nanjing 210028, China.

Published: February 2025


Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Hexabromocyclododecane (HBCD), a brominated flame retardant, is linked to various health implications, including prostate cancer. This study explored the molecular mechanisms and potential biomarkers associated with HBCD exposure using data from the Comparative Toxicogenomics Database (CTD) and The Cancer Genome Atlas (TCGA). A total of 7,147 differentially expressed genes (DEGs) and 46 differentially expressed miRNAs were identified, with significant enrichment in cancer-related pathways and xenobiotic metabolism. Protein-protein interaction (PPI) network construction and enrichment analyses revealed four hub genes: DNAJC12, PKMYT1, RRM2, and SLC12A5. These genes displayed notable expression changes in response to HBCD exposure and were strongly correlated with survival outcomes in prostate cancer patients, as demonstrated by Cox regression and ROC curve analyses. Additionally, miRNA correlation analyses indicated robust positive associations, highlighting a coordinated regulatory network. Experimental expression analyses on HBCD-treated cell lines further validated these findings. This study sheds light on the significant impact of HBCD on gene and miRNA expression in prostate cancer, emphasizing the potential of the identified hub genes and miRNAs as prognostic biomarkers and therapeutic targets. By elucidating the pathways and regulatory networks influenced by HBCD, the findings provide a foundation for developing strategies to mitigate its carcinogenic effects and improve outcomes for prostate cancer patients.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11788417PMC
http://dx.doi.org/10.1093/toxres/tfaf016DOI Listing

Publication Analysis

Top Keywords

prostate cancer
20
hbcd exposure
12
response hbcd
8
differentially expressed
8
hub genes
8
outcomes prostate
8
cancer patients
8
cancer
6
hbcd
6
prostate
5

Similar Publications

Importance: Multiparametric magnetic resonance imaging (MRI), with or without prostate biopsy, has become the standard of care for diagnosing clinically significant prostate cancer. Resource capacity limits widespread adoption. Biparametric MRI, which omits the gadolinium contrast sequence, is a shorter and cheaper alternative offering time-saving capacity gains for health systems globally.

View Article and Find Full Text PDF

Objective: This study aims to systematically evaluate the inter- and intra-observer agreement regarding lesions with uncertain malignancy potential in Ga-68 PSMA PET/CT imaging of prostate cancer patients, utilizing the PSMA-RADS 2.0 classification system, and to emphasize the malignancy evidence associated with these lesions.

Methods: We retrospectively reviewed Ga-68 PSMA PET/CT images of patients diagnosed with prostate cancer via histopathology between December 2016 and November 2023.

View Article and Find Full Text PDF

Influence of life expectancy on shared decision-making for prostate cancer screening.

Cancer Causes Control

September 2025

Department of Population Health Sciences, Weill Cornell Medicine, New York, NY, USA.

Purpose: The U.S. Preventive Services Task Force recommends that men aged 55-69 years undergo shared decision-making (SDM) regarding prostate cancer (PCa) screening, and routine screening is not recommended for older men or those with limited life expectancy.

View Article and Find Full Text PDF

Oligomeric proanthocyanidins (OPCs), condensed tannins found plentiful in grape seeds and berries, have higher bioavailability and therapeutic benefits due to their low degree of polymerization. Recent evidence places OPCs as effective modulators of cancer stem cell (CSC) plasticity and tumor growth. Mechanistically, OPCs orchestrate multi-pathway inhibition by destabilizing Wnt/β-catenin, Notch, PI3K/Akt/mTOR, JAK/STAT3, and Hedgehog pathways, triggering β-catenin degradation, silencing stemness regulators (OCT4, NANOG, SOX2), and stimulating tumor-suppressive microRNAs (miR-200, miR-34a).

View Article and Find Full Text PDF