Mediation of intracellular Ca2+ in the phospholipase A2-induced cell proliferation in human neuroblastoma cells.
- Author:
Jung Ae KIM
1
;
Yong Soo LEE
Author Information
1. Department of Physiology, College of Pharmacy, Yeungnam University, Kyongsan 712-749, Korea.
- Publication Type:Original Article
- Keywords:
Phospholipase A2;
Human neuroblastoma cells;
Cell proliferation;
Intracellular Ca2+
- MeSH:
Arachidonic Acid;
Cell Proliferation*;
Humans*;
Melitten;
Negotiating*;
Neuroblastoma*;
Phospholipases A2;
Phospholipases*;
Quinacrine
- From:The Korean Journal of Physiology and Pharmacology
1998;2(4):411-417
- CountryRepublic of Korea
- Language:English
-
Abstract:
The role of phospholipase A2 (PLA2) in tumor cell growth was investigated using SK-N-MC human neuroblastoma cells. 4-Bromophenacyl bromide (BPB) and mepacrine (Mep), known PLA2 inhibitors, suppressed growth of the tumor cells in a dose-dependent manner without a significant cytotoxicity. Melittin (Mel), a PLA2 activator, enhanced the cell growth in a concentration-dependent fashion. The growth-enhancing effects of Mel were significantly reversed by the co-treatment with PLA2 inhibitors. In addition, Mel induced intracellular Ca2+ release from internal stores like as did serum, a known intracellular Ca2+ agonist in the tumor cells. Intracellular Ca2+ release induced by these agonists was significantly blocked by PLA2 inhibitors at growth-inhibitory concentrations. Arachidonic acid (AA), a product of the PLA2-catalyzed reaction, induced cell growth enhancement and intracellular Ca2+ release. These effects of AA were significantly blocked by BAPTA/AM, an intracellular Ca2+ chelator. Taken together, these results suggest that the modulation of PLA2 activity may be one of the regulatory mechanisms of cell growth in human neuroblastoma cells. Intracellular Ca2+ may act as a key mediator in the PLA2-induced growth regulation.
