The Influence of β-Carotene and Its Liposomal Form on the Expression of EMT Markers and Androgen-Dependent Pathways in Different Prostate Cell Lines

Joanna Dulińska-Litewka*, Kacper Dykas, Stanisław Boznański, Przemysław Hałubiec, Marta Kaczor-Kamińska, Jacek Zagajewski, Torsten Bohn, Gracjan Wątor

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

Abstract

Prostate cancer (PCa) is the most common malignancy in men. Although the prognosis in the early stages is good, the treatment of advanced PCa remains a formidable challenge. Even after an initial response to hormone therapy or chemotherapy, recurrences are frequent and resistance to any systemic treatment is common. β-Carotene (BC), a plant-derived tetraterpene, is known for its antioxidant capacity and can modulate multiple cellular signaling pathways, potentially affecting androgen synthesis. We investigated the influence of BC (dissolved in EtOH/THF with a cell culture medium or encapsulated in liposomes (LP-BCs)) on the viability, migration potential, and connective tissue cleavage capabilities of several PCa cell lines (Du145, LNCaP, PC-3, and 22Rv1) and a healthy prostate model (RWPE cells). BC significantly reduced the proliferative capacity of all investigated cell lines at various concentrations (1.5–30 µM) and decreased cell migration. However, it significantly increased the expression of epidermal–mesenchymal transition (EMT) master proteins in all cancer cell lines and RWPE (p < 0.05) These effects were not observed with LP-BCs. This study suggests that LP-BCs, with their higher antiproliferative capabilities and pronounced inhibition of the EMT, may be a more effective form of possible PCa prevention or treatment than the free form. LPs may also modulate lipid metabolism in PCa cells.

Original languageEnglish
Article number902
JournalAntioxidants
Volume13
Issue number8
DOIs
Publication statusPublished - 25 Jul 2024

Keywords

  • androgens
  • carotenoids
  • epithelial–mesenchymal transition
  • lipid metabolism
  • nuclear receptors
  • prostate cancer

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