Orostachys japonicus induce p53-dependent cell cycle arrest through the MAPK signaling pathway in OVCAR-3 human ovarian cancer cells

Kyung Sun Lee, Suhng Wook Kim, Hyeong Seon Lee

Research output: Contribution to journalArticle

Abstract

Orostachys japonicus (O. japonicus) is utilized as a traditional medicine for patients with various diseases. This study investigated the effect of the ethyl acetate fraction from O. japonicus extract (OJE) on the growth inhibition of OVCAR-3 human ovarian cancer cells demonstrated to inhibit cell growth and arrest the cell cycle in OVCAR-3 cells by blocking the sub-G1 phase and decreasing cyclin E1/CDK2 expression. Cell cycle arrest was connected to the increased expression of the cell cycle regulating factors p53 and p21. Apoptosis was initiated through the intrinsic pathway by up-regulating the expression of the Bcl-2/Bax ratio and down-regulating the expression of pro-caspase-3. Furthermore, OJE treatment elicited p-p38 activation and p-ERK1/2 inhibition. In conclusion, our results demonstrated that OJE reduced the growth of OVCAR-3 human ovarian cancer cells mediated by arrest of the cell cycle and regulation of MAPK signaling pathways.

Original languageEnglish
Pages (from-to)2395-2401
Number of pages7
JournalFood Science and Nutrition
Volume6
Issue number8
DOIs
Publication statusPublished - 2018 Nov 1

Fingerprint

Orostachys japonica
ovarian neoplasms
Cell Cycle Checkpoints
Ovarian Neoplasms
extracts
Growth
cyclins
caspase-3
traditional medicine
interphase
growth retardation
Cyclins
cell growth
cell cycle
G1 Phase
Traditional Medicine
apoptosis
Caspase 3
Cell Cycle
Apoptosis

Keywords

  • apoptosis
  • cell cycle
  • Orostachys japonicus
  • ovarian cancer cells

ASJC Scopus subject areas

  • Food Science

Cite this

Orostachys japonicus induce p53-dependent cell cycle arrest through the MAPK signaling pathway in OVCAR-3 human ovarian cancer cells. / Lee, Kyung Sun; Kim, Suhng Wook; Lee, Hyeong Seon.

In: Food Science and Nutrition, Vol. 6, No. 8, 01.11.2018, p. 2395-2401.

Research output: Contribution to journalArticle

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