These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Activation of phospholipase C-γ1 and translocation of phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase contribute to GL-V9-induced apoptosis in human gastric cancer cells. Author: Zhao K, Li G, Yao Y, Zhou Y, Li Z, Guo Q, Lu N. Journal: Exp Cell Res; 2017 Jul 01; 356(1):8-19. PubMed ID: 28412247. Abstract: Gastric cancer is the most common type of tumor in developing countries and the fourth most frequently diagnosed cancer worldwide. Here, we demonstrated the apoptotic effects of GL-V9 on several human gastric cancer cells and selected MGC-803 cells to uncover the underlying mechanism. GL-V9 elevated Bax/Bcl-2 ratio, abated mitochondrial membrane potential and triggered the onset of apoptotic execution in MGC-803 cells. Our research revealed that CHOP silencing could not inhibit apoptosis, neither could it block Ca2+ release, suggesting that GL-V9-induced apoptosis was independent of CHOP. Furthermore, GL-V9 increased mitochondrial Ca2+ uptake through 1,4,5-triphosphate (IP3) receptor via the activation of phospholipase C-γ1 and the translocation of phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase from nucleus to endoplasmic reticulum. Moreover, in-vivo studies indicated that GL-V9 exhibited significant MGC-803 xenografts regression in nude mice with low systemic toxicity. In conclusion, GL-V9 could induce apoptosis in gastric cancer cells, and would be a promising therapeutical agent against gastric cancer.[Abstract] [Full Text] [Related] [New Search]