Geraniol induces cooperative interaction of apoptosis and autophagy to elicit cell death in PC-3 prostate cancer cells

Su Hwa Kim, Eun Jung Park, Chae Ryun Lee, Jung Nyeo Chun, Nam Hyuk Cho, In Gyu Kim, Sanghoon Lee, Tae Woo Kim, Hyun Ho Park, Insuk So, Ju Hong Jeon

Research output: Contribution to journalArticle

44 Citations (Scopus)

Abstract

Geraniol, an acyclic dietary monoterpene, suppresses prostate cancer growth and enhances docetaxel chemosensitivity in cultured cell or xenograft tumor models. However, the mechanisms of the geraniol action against prostate cancer are largely unknown. In this study, we investigated the cellular and molecular mechanisms of geraniol-induced cell death in PC-3 prostate cancer cells. Among the examined structurally and functionally similar monoterpenes, geraniol potently induced apoptosis and autophagy. Although independent processes, apoptosis and autophagy acted as cooperative partners to elicit geraniol-induced cell death in PC-3 cells. At a molecular level, geraniol inhibited AKT signaling and activated AMPK signaling, resulting in mTOR inhibition. Combined treatment of AKT inhibitor and AMPK activator markedly suppressed cell growth compared to either treatment alone. Our findings provide insight into future investigations that are aimed at elucidating the role of apoptosis and autophagy in prostate cancer therapy and at developing anticancer strategies co-targeting AKT and AMPK.

Original languageEnglish
Pages (from-to)1683-1690
Number of pages8
JournalInternational Journal of Oncology
Volume40
Issue number5
DOIs
Publication statusPublished - 2012 May 1

Fingerprint

Autophagy
Prostatic Neoplasms
Cell Death
Apoptosis
AMP-Activated Protein Kinases
Monoterpenes
docetaxel
Growth
Heterografts
geraniol
Cultured Cells
Neoplasms

Keywords

  • Apoptosis
  • Autophagy
  • Cell death
  • Geraniol
  • Prostate cancer

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Geraniol induces cooperative interaction of apoptosis and autophagy to elicit cell death in PC-3 prostate cancer cells. / Kim, Su Hwa; Park, Eun Jung; Lee, Chae Ryun; Chun, Jung Nyeo; Cho, Nam Hyuk; Kim, In Gyu; Lee, Sanghoon; Kim, Tae Woo; Park, Hyun Ho; So, Insuk; Jeon, Ju Hong.

In: International Journal of Oncology, Vol. 40, No. 5, 01.05.2012, p. 1683-1690.

Research output: Contribution to journalArticle

Kim, SH, Park, EJ, Lee, CR, Chun, JN, Cho, NH, Kim, IG, Lee, S, Kim, TW, Park, HH, So, I & Jeon, JH 2012, 'Geraniol induces cooperative interaction of apoptosis and autophagy to elicit cell death in PC-3 prostate cancer cells', International Journal of Oncology, vol. 40, no. 5, pp. 1683-1690. https://doi.org/10.3892/ijo.2011.1318
Kim, Su Hwa ; Park, Eun Jung ; Lee, Chae Ryun ; Chun, Jung Nyeo ; Cho, Nam Hyuk ; Kim, In Gyu ; Lee, Sanghoon ; Kim, Tae Woo ; Park, Hyun Ho ; So, Insuk ; Jeon, Ju Hong. / Geraniol induces cooperative interaction of apoptosis and autophagy to elicit cell death in PC-3 prostate cancer cells. In: International Journal of Oncology. 2012 ; Vol. 40, No. 5. pp. 1683-1690.
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AB - Geraniol, an acyclic dietary monoterpene, suppresses prostate cancer growth and enhances docetaxel chemosensitivity in cultured cell or xenograft tumor models. However, the mechanisms of the geraniol action against prostate cancer are largely unknown. In this study, we investigated the cellular and molecular mechanisms of geraniol-induced cell death in PC-3 prostate cancer cells. Among the examined structurally and functionally similar monoterpenes, geraniol potently induced apoptosis and autophagy. Although independent processes, apoptosis and autophagy acted as cooperative partners to elicit geraniol-induced cell death in PC-3 cells. At a molecular level, geraniol inhibited AKT signaling and activated AMPK signaling, resulting in mTOR inhibition. Combined treatment of AKT inhibitor and AMPK activator markedly suppressed cell growth compared to either treatment alone. Our findings provide insight into future investigations that are aimed at elucidating the role of apoptosis and autophagy in prostate cancer therapy and at developing anticancer strategies co-targeting AKT and AMPK.

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