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A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
Published on: March 6, 2018
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Persistent organic pollutants promote aggressiveness in prostate cancer
Julio Buñay1,2,3, Myriam Kossai2,4, Christelle Damon-Soubeyrant1,2,3
1Université Clermont Auvergne, iGReD, CNRS UMR 6293, INSERM U1103, 28, place Henri Dunant, BP38, 63001, Clermont-Ferrand, France.
Oncogene
|August 16, 2023
Summary
Exposure to persistent organic pollutants (POPs) like dioxin and PCB-153 promotes prostate cancer growth and metastasis. This study identifies Acetyl-CoA Acetyltransferase-1 (ACAT1) deregulation as a key mechanism driving these effects.
Area of Science:
- Environmental Health
- Oncology
- Biochemistry
Background:
- Persistent organic pollutants (POPs), including dioxin and PCB-153, are linked to increased cancer incidence and aggressiveness.
- While dioxin's role in some cancers is known, its impact on prostate cancer requires further investigation.
- Prostate cancer progression may be influenced by dioxin and PCB-153 exposure.
Purpose of the Study:
- To investigate the effects of low-dose dioxin and PCB-153 exposure on prostate cancer progression in ex vivo and in vivo models.
- To identify molecular mechanisms underlying POP-induced prostate cancer aggressiveness.
- To validate findings in human prostate cancer datasets and patient samples.
Main Methods:
- Exposure of prostate cancer cells and Ptenpc-/- mice to low doses of dioxin and PCB-153.
- Assessment of cancer cell growth, metastasis, and histopathological changes.
- Analysis of Acetyl-CoA Acetyltransferase-1 (ACAT1) expression and its role in dioxin-mediated effects.
- Examination of public prostate cancer datasets and a cohort of Agent Orange-exposed veterans.
Main Results:
- Dioxin and PCB-153 exposure enhanced prostate cancer cell growth and metastasis ex vivo and in vivo.
- Histopathological carcinoma-like patterns were observed in exposed Ptenpc-/- mice.
- ACAT1 upregulation was identified as a mediator of dioxin's effect on cell migration.
- ACAT1 and ketone body pathway enzyme deregulation was confirmed in advanced human prostate cancer and Agent Orange-exposed veterans.
Conclusions:
- Dioxin and PCB-153 exposure promote a prometastatic program in prostate tumors.
- ACAT1 deregulation is a critical event in dioxin-induced prostate cancer progression.
- This research highlights POPs as environmental risk factors for aggressive prostate cancer.
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