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April 13, 2026Journal of Toxicology0 citationsOpen Access

Phillyrin Modulates AMPK‐Associated Cellular Responses and Migration in PC3 Prostate Cancer Cells

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CLCheng-Hsin LuCWChun-Hsien WuPHPei‐Fang Hsieh

Key Points

  • The research aims to assess the impact of phillyrin on PC3 prostate cancer cells and to explore related cellular responses.
  • PC3 prostate cancer cells were treated with phillyrin at concentrations of 1, 2.5, and 5 μM for 24 hours.
  • A wound-healing assay was used to measure cell migration.
  • Western blotting and immunofluorescence analyzed AMPK-related proteins and epithelial-mesenchymal transition markers.
  • Pharmacological inhibition with Compound C was applied to evaluate the role of AMPK in phillyrin's effects.
  • Phillyrin treatment decreased the migratory ability of PC3 cells without causing cell death.
  • There was a reduction in expression of α-smooth muscle actin, Snail, and Slug, while E-cadherin expression increased.
  • SIRT1 and NRF1 protein levels were elevated following phillyrin treatment, along with changes in AMPK expression.
  • Inhibition of AMPK activity with Compound C negated phillyrin's effects on EMT markers.

Abstract

Males with prostate cancer exhibit substantial mortality and metastasis; however, few effective treatment strategies are available for advanced prostate cancer. Phillyrins (PHNs) are lignan glycosides that have been reported to exhibit diverse biological activities, including potential anticancer effects. We aimed (1) to assess the effect of PHN on PC3 prostate cancer cells and (2) to examine cellular responses associated with its activity. To assess the effects of PHN, it was exposed to various concentrations of PHN (1, 2.5, and 5 μM) for 24 h. A wound‐healing assay was performed to evaluate cell migration. Western blotting and immunofluorescence were used to investigate the expression of adenosine monophosphate–activated protein kinase (AMPK)–associated proteins and transcription factors involved in epithelial–mesenchymal transition (EMT). PHN exposure was associated with reduced migratory capacity of PC3 cells under noncytotoxic conditions. PHN exposure was associated with decreased α‐smooth muscle actin, Snail, and Slug expression while increasing E‐cadherin expression. Sirtuin 1 (SIRT1) and nuclear respiratory factor 1 (NRF1) protein levels were upregulated in PHN‐treated cells, accompanied by changes in AMPK protein expression. Pharmacological inhibition with Compound C attenuated PHN‐associated changes in EMT‐related marker expression in PC3 cells. Thus, PHN exposure may influence EMT‐associated phenotypes in PC3 cells, potentially involving AMPK‐associated signaling.

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Cite This Study

Lu et al. (2026) studied this question.

synapsesocial.com/papers/69dc89473afacbeac03eb204https://doi.org/10.1155/jt/2022957
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