• Title/Summary/Keyword: %24BCl_3%2FAr%24

Search Result 2, Processing Time 0.016 seconds

Cisplatin Suppresses Proliferation of Ovarian Cancer Cells through Inhibition Akt and Modulation MAPK Pathways (Cisplatin의 난소암 세포 증식 억제에 관한 신호 전달 기전)

  • Choi, Jae-Sun
    • Korean Journal of Clinical Laboratory Science
    • /
    • v.52 no.1
    • /
    • pp.62-68
    • /
    • 2020
  • Cisplatin (CDDP) is a chemotherapy agent used for patients with ovarian cancers. CDDP activates multiple signaling pathways, which causes various cellular reactions according to the type of cancer cells. Therefore, it is difficult to clearly conclude its signaling pathways. The purpose of this study is to determine the role of the signal protein of Akt/ERK1/2 and MAPK by CDDP-induced apoptosis in ovarian cancer cells (SKOV3). As a result, the number of apoptosis increased according to the TUNEL assay, and flow cytometric analysis confirmed that the percentage of sub-G1 early apoptosis was 8.73% higher than the control. The PARP and caspase-3 activity that appeared in the process of apoptosis was increased and the Bcl-2 expression was decreased. It was verified that the Akt and ERK1/2 activity was decreased, and p38 and JNK activity increased in a time dependent fashion. In conclusion, these results demonstrate that cisplatin inhibits the proliferation of ovarian cancer cells by inhibiting Akt activity and induces apoptosis by modulating the MAPK signaling pathway. However, a decrease in the ERK1/2 activity by CDDP was the opposite result to the result shown from the HeLa cells. For this reason, further research on signaling pathways is necessary. These results are expected to be useful for ovarian cancer treatment strategies targeting the MAPK pathway.

Chestnut extract induces apoptosis in AGS human gastric cancer cells

  • Lee, Hyun-Sook;Kim, Eun-Ji;Kim, Sun-Hyo
    • Nutrition Research and Practice
    • /
    • v.5 no.3
    • /
    • pp.185-191
    • /
    • 2011
  • In Korea, chestnut production is increasing each year, but consumption is far below production. We investigated the effect of chestnut extracts on antioxidant activity and anticancer effects. Ethanol extracts of raw chestnut (RCE) or chestnut powder (CPE) had dose-dependent superoxide scavenging activity. Viable numbers of MDA-MD-231 human breast cancer cells, DU145 human prostate cancer cells, and AGS human gastric cancer cells decreased by 18, 31, and 69%, respectively, following treatment with $200{\mu}g/mL$ CPE for 24 hr. CPE at various concentrations ($0-200{\mu}g/mL$) markedly decreased AGS cell viability and increased apoptotic cell death dose and time dependently. CPE increased the levels of cleaved caspase-8, -7, -3, and poly (ADP-ribose) polymerase in a dose-dependent manner but not cleaved caspase-9. CPR exerted no effects on Bcl-2 and Bax levels. The level of X-linked inhibitor of apoptosis protein decreased within a narrow range following CPE treatment. The levels of Trail, DR4, and Fas-L increased dose-dependently in CPE-treated AGS cells. These results show that CPE decreases growth and induces apoptosis in AGS gastric cancer cells and that activation of the death receptor pathway contributes to CPE-induced apoptosis in AGS cells. In conclusion, CPE had more of an effect on gastric cancer cells than breast or prostate cancer cells, suggesting that chestnuts would have a positive effect against gastric cancer.