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An Orthotopic Murine Model of Human Prostate Cancer Metastasis
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THE IMPACT OF ALCOHOL ON PRO-METASTATIC N-GLYCOSYLATION IN PROSTATE CANCER.

A V Kubyshkin1, I I Fomochkina1, A M Petrosyan2

  • 1Medical Academy named after S.I. Georgievsky, V.I. Vernadsky Crimean Federal University, Lenin Avenue 5/7, Simferopol, Russia; 295051.

Krimskii Zhurnal Eksperimental'Noi I Klinicheskoi Meditsiny = Kryms'Kyi Zhurnal Eksperymental'Noi Ta Klinichnoi Medytsyny = Crimean Journal of Experimental and Clinical Medicine
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PubMed
Summary

Chronic alcohol abuse promotes prostate cancer (PCa) progression by disrupting the Golgi complex, leading to altered protein glycosylation and increased metastasis. This study reveals alcohol

Keywords:
N-glycosylationalcoholdisorganization of Golgi complexmetastasisprostate cancer

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Area of Science:

  • Cell Biology
  • Cancer Research
  • Biochemistry

Background:

  • Chronic alcohol abuse is a risk factor for prostate cancer (PCa) progression.
  • Golgi complex fragmentation correlates with PCa progression.
  • Ethanol (EtOH) disrupts Golgi organization and protein localization.

Purpose of the Study:

  • To investigate the mechanism by which alcohol abuse promotes PCa progression.
  • To explore the role of Golgi fragmentation and altered glycosylation in alcohol-mediated tumor promotion.
  • To examine the relationship between Golgi morphology, MGAT3, and PCa in patient specimens.

Main Methods:

  • High-resolution microscopy to observe Golgi morphology in cell lines.
  • Analysis of N-acetylglucosaminyltransferase-III (MGAT3) and MGAT5 expression and localization.
  • Assessment of Golgi morphology and MGAT3 in human PCa patient specimens.
  • In vitro studies on EtOH effects on MGAT3, MGAT5, matriptase, and integrins.

Main Results:

  • Alcohol exposure induced Golgi fragmentation in prostate cancer cells, mimicking advanced disease.
  • Androgen unresponsiveness correlated with decreased MGAT3 and increased MGAT5 activity.
  • Alcohol-induced Golgi fragmentation caused MGAT3 translocation from the Golgi to the cytoplasm.
  • Human PCa patients with alcohol dependence showed increased Golgi disorganization and MGAT3 cytoplasmic shift.
  • In vitro, EtOH downregulated MGAT3, activating MGAT5-mediated glycosylation and increasing pro-metastatic proteins.

Conclusions:

  • Alcohol consumption promotes PCa progression through Golgi complex disruption and altered N-glycosylation.
  • The study identifies a novel mechanism of alcohol-mediated tumor promotion involving MGAT3 and MGAT5.
  • Findings highlight the clinical relevance of alcohol use in PCa progression and suggest potential therapeutic targets.