Toosendanin induces caspase-dependent apoptosis through the p38 MAPK pathway in human gastric cancer cells
- Department of Gastrointestinal Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong (China)
- Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, Guangdong Institute of Gastroenterology, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong (China)
Highlights: • Toosendanin suppresses viability of various gastric cancer cell lines. • Toosendanin induces G{sub 1}/S cell cycle arrest followed by inhibiting proliferation of AGS and HGC-27 cells. • Toosendanin induces caspase-dependent apoptosis via p38 MAPK signaling pathway in AGS and HGC-27 cells. • Toosendanin can be a promising therapeutic compound for gastric cancer therapy. Although many advances have been made in the treatment of gastric cancer (GC), numerous difficulties, such as the emergence of chemo-drug resistance, continue to lead to disappointing GC prognoses. Thus, novel alternative strategies are urgently needed. The use of natural products could be a viable option to treat GC. Toosendanin (TSN) is a triterpenoid derived from the bark of Melia toosendanin Sieb. et Zucc that has been shown to be highly cytotoxic to multiple cancer cells. As the underlying impact of TSN on GC and its molecular mechanism remain poorly understood, in this study, we performed a series of experiments involving the use of TSN to treat GC cells. In the present study, we showed that TSN suppressed cell viability, inhibited cell proliferation by causing G{sub 1}/S arrest and induced caspase-dependent apoptosis in AGS and HGC-27 cells. The possible mechanism of TSN-induced apoptosis may be associated with the activation of the p38 MAPK pathway. These results demonstrated the potential of TSN as a promising therapeutic compound to treat gastric cancer.
- OSTI ID:
- 23107824
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 505, Issue 1; Other Information: Copyright (c) 2018 Elsevier Inc. All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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