Cellular mechanisms of a new pyrazinone compound that induces apoptosis in SKOV-3 cells.

نویسندگان

  • Guan Wang
  • Meng-Ying Jiang
  • Ying Meng
  • Hong-Rui Song
  • Wei Shi
چکیده

We screened a small molecular library that was designed and independently synthesized in vitro and found a new drug (MY-03-01) that is active against ovarian cancer. We established that MY-03-01 effectively inhibited SKOV-3 cell survival in a dose-dependent manner, based on cell viability rates, and that it not only induced SKOV-3 apoptosis by itself, but also did so synergistically with paclitaxel. Secondly, when MY-03-01 was applied at 40 μM, its hemolytic activity was less than 10%, compared with the control, and there was almost no damage to normal cells at this concentration. In addition, we used DAPI staining and flow cytometry to show that MY- 03-01 could significantly induce apoptosis of SKOV-3 cells. Finally, we found that MY-03-01 likely induced SKOV-3 apoptosis by activating caspase3 and caspase9 through the mitochondrial pathway.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Econazole Nitrate Induces Apoptosis in MCF-7 Cells via Mitochondrial and Caspase Pathways

Econazole nitrate (EN), a synthetic compound, is now in use as a routine antifungal drug. EN was shown to have antitumor effect, the tumor cell killing mechanisms, however, remain unclear. In this research, the apoptosis-inducing effect of EN on MCF-7 cells was investigated. The results showed that EN inhibited the proliferation of MCF-7 cells in a time- and dose-dependent manner by MTT method ...

متن کامل

Econazole Nitrate Induces Apoptosis in MCF-7 Cells via Mitochondrial and Caspase Pathways

Econazole nitrate (EN), a synthetic compound, is now in use as a routine antifungal drug. EN was shown to have antitumor effect, the tumor cell killing mechanisms, however, remain unclear. In this research, the apoptosis-inducing effect of EN on MCF-7 cells was investigated. The results showed that EN inhibited the proliferation of MCF-7 cells in a time- and dose-dependent manner by MTT method ...

متن کامل

Glycyrrhetinic Acid Induces Apoptosis in Leukemic HL60 Cells Through Upregulating of CD95/ CD178

Acute leukemia is characterized by the accumulation of neoplastic cells in the bone marrow and peripheral blood. Currently, chemotherapy and differentiating agents have been used for the treatment of leukemia. Recently, plant extracts, either alone or in combination with chemo agents, have been proposed to be used for the treatment of cancers. The aim of the present research was to study the cy...

متن کامل

Epigallocatechin-3-Gallate Induces Apoptosis through Up-regulation of Bax and Down-regulation of Bcl-2 in Prostate Cancer Cell Line

Background and Aims: Epigallocatechin-3-gallate (EGCG) is a polyphenolic compound from green tea, which its anticancer effects on many types of cancers have been confirmed, but the molecular mechanism by which EGCG induces apoptosis remains unknown. The aim of the present study was to investigate anti-proliferative properties and apoptotic signaling pathway of EGCG on PC3 human prostate cancer ...

متن کامل

Gallic Acid Inhibits Proliferation and Induces Apoptosis in Lymphoblastic Leukemia Cell Line (C121)

AbstractLeukemia is known as the world’s fifth most prevalent cancer. New cytotoxic drugs have created considerable progress in the treatment, but side effects are still the important cause of mortality. Plant derivatives have been recently considered as important sources for the treatment of various diseases, including cancer. Gallic acid (GA) is a polyhydroxyphenolic compound with a wide rang...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Asian Pacific journal of cancer prevention : APJCP

دوره 15 2  شماره 

صفحات  -

تاریخ انتشار 2014