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Tributyltin-dysregulated periprostatic adipose tissue enhances prostate cell survival and migration, implicating the C-C motif chemokine receptor 3.

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Related Experiment Video

Updated: Jan 13, 2026

Generation of Prostate Cancer Cell Models of Resistance to the Anti-mitotic Agent Docetaxel
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Tributyltin Protumorigenic Effects Targeting Prostate Cancer Cell Metabolism, Proliferation, Migration, and Invasion.

Mariana Feijó1, Luís P Brás2, Catarina M D Serra1

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|January 6, 2026
PubMed
Summary

Environmental tributyltin (TBT), an endocrine-disrupting chemical, promotes prostate cancer (PCa) progression. TBT disrupts cell metabolism and enhances PCa cell proliferation, migration, and invasion, raising concerns about environmental impacts on cancer development.

Keywords:
5α‐dihydrotestosteroneendocrine‐disrupting‐chemicalslow‐density lipoproteinprostate cancertributyltin

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Area of Science:

  • Environmental Science
  • Oncology
  • Endocrinology

Background:

  • Prostate cancer (PCa) is an endocrine-related malignancy influenced by both hormonal and extrinsic factors.
  • Endocrine-disrupting chemicals (EDCs) are environmental compounds that may increase PCa risk.
  • Tributyltin (TBT) is an EDC found in antifouling paints with known androgenic and obesogenic properties.

Purpose of the Study:

  • To investigate the effects of TBT on key cancer hallmarks in prostate cells.
  • To evaluate TBT's impact on prostate cancer cell viability, metabolism, proliferation, migration, and invasion.
  • To explore the mechanisms underlying TBT's influence on prostate cancer progression using in vitro and in vivo models.

Main Methods:

  • In vitro studies exposed androgen-sensitive (LNCaP) and androgen-insensitive (PC3) PCa cells to varying concentrations of TBT.
  • Cellular responses were analyzed following treatment with TBT alone, or in combination with bicalutamide, LDL, and DHT.
  • In vivo studies involved administering TBT to Wistar rats over a 45-day period.

Main Results:

  • TBT disrupted glycolytic flux and lipid handling in prostate cells, significantly enhancing proliferative activity.
  • Exposure to TBT stimulated the migration and invasion capabilities of LNCaP cells.
  • The effects of TBT on glucose consumption and proliferation were partially attenuated by bicalutamide; lower TBT concentrations promoted viability, proliferation, and invasion when combined with LDL and DHT.

Conclusions:

  • Tributyltin (TBT) acts as a potential inducer of prostate cancer progression and aggressiveness.
  • EDCs like TBT play a significant role in the prostate carcinogenic process.
  • Further research is warranted to understand the full impact of environmental EDCs on prostate cancer development and progression.