ArticleMedical sciences (Basel, Switzerland)2025
Obesogenic Dysregulation of Human Periprostatic Adipose Tissue Promotes the Viability of Prostate Cells and Reduces Their Sensitivity to Docetaxel and Cabazitaxel.
Article in Medical sciences (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Authors and funding
10 authors.
Funding
Abstract
backgroundPeriprostatic adipose tissue (PPAT) has been shown to play a significant role in prostate cancer (PCa) development and progression. This relationship is further exacerbated by obesity, as PPAT-secreted factors increase PCa aggressiveness and have also been implicated in chemotherapy resistance. Therefore, identifying the molecular mediators of PPAT-prostate interorgan communication and the factors that disrupt this crosstalk is pivotal for better disease management. Obesogens, i.e., endocrine-disrupting chemicals that dysregulate adipose tissue towards an "obese" phenotype, have recently been implicated in disrupting this crosstalk, with an impact on prostate cell fate.
objectivesThis study aimed to investigate whether obesogenic dysregulation of human PPAT secretory activity affects PCa cell viability and their response to docetaxel and cabazitaxel. METHODS/
resultsThrough
conclusionsThis study provides preliminary evidence that lays the groundwork for future investigations, dissecting the molecular pathways underpinning prostate carcinogenesis and resistance to chemotherapy induced by obesogen-dysregulated PPAT.
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