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.
Highlights
Human ovarian cancer is a major cause of gynecological cancer death in women
Various studies have revealed that kaempferol and quercetin lead to apoptosis using the natural products in various human cancer cells (Lee, Szcsepanski, & Lee, 2008; Yoshida et al, 2008)
These results suggest that cell cycle arrest induced by O. japonicus extract (OJE) treatment might be mediated through the down-regulation of cyclin E1/CDK2 expression and up-regulation of p53 and p21 expression
Summary
Human ovarian cancer is a major cause of gynecological cancer death in women. Surgical castration and chemotherapy are mainly used in cancer treatments, including ovarian cancer (Jemal et al, 2008; Shirali et al, 2013). Orostachys japonicus is reported to contain 16 types of flavonoid contents They have been confirmed to have antioxidant activity using DPPH assay (Lee et al, 2011). There are no reports on anti-cancer activity of the ethyl acetate fraction from O. japonicus extract (OJE) in human ovarian cancer cell lines. We investigated the effect of OJE on cell proliferation as well as its apoptotic pathway and cell cycle progression in the OVCAR-3 human ovarian cancer cell line.
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