DAG/PKCδ and IP3/Ca2+/CaMK IIβ Operate in Parallel to Each Other in PLCγ1-Driven Cell Proliferation and Migration of Human Gastric Adenocarcinoma Cells, through Akt/mTOR/S6 Pathway

作者：Dai, Lianzhi; Zhuang, Luhua; Zhang, Bingchang; Wang, Fen; Chen, Xiaolei; Xia, Chun^*; Zhang, Bing

来源：International Journal of Molecular Sciences, 2015, 16(12): 28510-28522.

DOI：10.3390/ijms161226116

• PLC1
• DAG
• PKC
• IP3
• Ca2+
• CaMK II
• Akt
• mTOR
• S6
• cell proliferation
• migration
• human gastric adenocarcinoma cells

Phosphoinositide specific phospholipase C (PLC) activates diacylglycerol (DAG)/protein kinase C (PKC) and inositol 1,4,5-trisphosphate (IP3)/Ca2+/calmodulin-dependent protein kinase II (CaMK II) axes to regulate import events in some cancer cells, including gastric adenocarcinoma cells. However, whether DAG/PKC and IP3/Ca2+/CaMK II axes are simultaneously involved in PLC1-driven cell proliferation and migration of human gastric adenocarcinoma cells and the underlying mechanism are not elucidated. Here, we investigated the role of DAG/PKC or CaMK II in PLC1-driven cell proliferation and migration of human gastric adenocarcinoma cells, using the BGC-823 cell line. The results indicated that the inhibition of PKC and CaMK II could block cell proliferation and migration of BGC-823 cells as well as the effect of inhibiting PLC1, including the decrease of cell viability, the increase of apoptotic index, the down-regulation of matrix metalloproteinase (MMP) 9 expression level, and the decrease of cell migration rate. Both DAG/PKC and CaMK II triggered protein kinase B (Akt)/mammalian target of rapamycin (mTOR)/S6 pathway to regulate protein synthesis. The data indicate that DAG/PKC and IP3/Ca2+/CaMK II operate in parallel to each other in PLC1-driven cell proliferation and migration of human gastric adenocarcinoma cells through Akt/mTOR/S6 pathway, with important implication for validating PLC1 as a molecular biomarker in early gastric cancer diagnosis and disease surveillance.

• 出版日期2015-12
• 单位厦门大学