Antitumoral effects of γCdcPLI, a PLA2 inhibitor from Crotalus durissus collilineatus via PI3K/Akt pathway on MDA-MB-231 breast cancer cell

Sci Rep. 2017 Aug 1;7(1):7077. doi: 10.1038/s41598-017-07082-2.

Abstract

Phospholipases A2 (PLA2s) overexpression is closely associated with the malignant potential of breast cancers. Here, we showed for the first the antitumoral effects of γCdcPLI, a PLA2 inhibitor from Crotalus durissus collilineatus via PI3K/Akt pathway on MDA-MB-231 cell. Firstly, γCdcPLI was more cytotoxic to MDA-MB-231 breast cancer cells than other cell lines (MCF-7, HeLa, PC3 and A549) and did not affect the viability of non-tumorigenic breast cell (MCF 10A). In addition, γCdcPLI induced modulation of important mediators of apoptosis pathways such as p53, MAPK-ERK, BIRC5 and MDM2. γCdcPLI decreased MDA-MB-231 adhesion, migration and invasion. Interestingly, the γCdcPLI also inhibited the adhesion and migration of endothelial cells and blocked angiogenesis by inhibiting tube formation by HUVECs in vitro and sprouting elongation on aortic ring assay ex vivo. Furthermore, γCdcPLI reduced the production of vascular endothelial growth factor (VEGF). γCdcPLI was also able to decrease PGE2 levels in MDA-MB-231 and inhibited gene and protein expression of the PI3K/Akt pathway. In conclusion, γCdcPLI showed in vitro antitumoral, antimestatatic and anti-angiogenic potential effects and could be an attractive approach for futures studies in cancer therapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / isolation & purification
  • Antineoplastic Agents / pharmacology*
  • Breast Neoplasms*
  • Cell Adhesion / drug effects
  • Cell Line, Tumor
  • Cell Movement / drug effects
  • Cell Survival / drug effects
  • Crotalid Venoms / chemistry
  • Endothelial Cells / drug effects
  • Humans
  • Lipoproteins / isolation & purification
  • Lipoproteins / pharmacology*
  • Models, Biological
  • Neovascularization, Pathologic
  • Oncogene Protein v-akt / metabolism*
  • Phosphatidylinositol 3-Kinase / metabolism*
  • Phospholipase A2 Inhibitors / isolation & purification
  • Phospholipase A2 Inhibitors / pharmacology*

Substances

  • Antineoplastic Agents
  • Crotalid Venoms
  • Lipoproteins
  • Phospholipase A2 Inhibitors
  • Phosphatidylinositol 3-Kinase
  • Oncogene Protein v-akt