Menthol induces cell-cycle arrest in PC-3 cells by down-regulating G2/M genes, including polo-like kinase 1

Su Hwa Kim, Sanghoon Lee, Stephen R. Piccolo, Kristina Allen-Brady, Eun Jung Park, Jung Nyeo Chun, Tae Woo Kim, Nam Hyuk Cho, In Gyu Kim, Insuk So, Ju Hong Jeon

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Menthol, a naturally occurring monoterpene, is used in foods, cosmetic products, and topical therapeutic preparations. It also exerts cytotoxic activity against several cancer cell types, including prostate cancer cells. However, little is known about the mechanism of menthol action against prostate cancer cells. In this study, we investigated the effect of menthol on the gene expression profile of PC-3 prostate cancer cells using DNA microarray analyses. Gene set enrichment analysis revealed that menthol primarily affects the expression of cell cycle-related genes. Subsequent experimental analyses validated that menthol induces G2/M arrest. Particularly, menthol markedly down-regulated polo-like kinase 1 (PLK1), a key regulator of G2/M phase progression and inhibited its downstream signaling. Our computational analyses and experimental validation provide a basis for future investigations that are aimed at elucidating the action of menthol on cell cycle control in prostate cancer cells.

Original languageEnglish
Pages (from-to)436-441
Number of pages6
JournalBiochemical and biophysical research communications
Volume422
Issue number3
DOIs
Publication statusPublished - 2012 Jun 8

Keywords

  • DNA microarray
  • Gene set enrichment analysis
  • Menthol
  • PLK1
  • Prostate cancer

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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    Kim, S. H., Lee, S., Piccolo, S. R., Allen-Brady, K., Park, E. J., Chun, J. N., Kim, T. W., Cho, N. H., Kim, I. G., So, I., & Jeon, J. H. (2012). Menthol induces cell-cycle arrest in PC-3 cells by down-regulating G2/M genes, including polo-like kinase 1. Biochemical and biophysical research communications, 422(3), 436-441. https://doi.org/10.1016/j.bbrc.2012.05.010