Open AccessESCIN MITIGATES HYPOXIA MIMICKING NCI-H23 CELLS THROUGH MODULATION OF MMPs, HIF-1α AND HIF-2α
Author(s) -
Panneer Selvam Chermakani,
Ganapasam Sudhandiran
Publication year - 2020
Publication title -
international journal of pharmacy and pharmaceutical sciences/international journal of pharmacy and pharmaceutical sciences
Language(s) - English
Resource type - Journals
eISSN - 2656-0097
pISSN - 0975-1491
DOI - 10.22159/ijpps.2020v12i12.39788
Subject(s) - matrix metalloproteinase , hypoxia (environmental) , chemistry , zymography , cancer research , extracellular matrix , microbiology and biotechnology , biochemistry , medicine , biology , oxygen , organic chemistry
Objective: The objective of the study is to investigate the effect of escin in hypoxia mimicked NCI-H23 cells through the modulation of matrix metalloproteinases (MMPs) 2 and 9.
Methods: In escin-treated NCI-H23 cells, adhesion, migration, and invasion were detected by the adhesion, wound healing, and Boyden chamber assays, respectively. The activation of proteinases was detected using zymography assay. The expressions of HIF-1α and HIF-2α were evaluated by immunoblot.
Results: In the present study, it was observed that escin suppressed chemically induced hypoxia condition and stimulated adhesion, migration, and invasion of NCI-H23 cells. Gelatin zymography assay showed that escin inhibited CoCl2 induced MMPs-2 and 9 activations in NCI-H23 cells. Furthermore, immunoblot analysis revealed that escin treatment decreased the expression of both HIF-1 and 2α in a dose-dependent manner under CoCl2 induced hypoxia condition.
Conclusion: Taken together, these results indicate that escin inhibits HIFs-α mediated MMPs-2 and 9 expressions, resulting in suppression of lung cancer cell invasion that is induced by chemically induced hypoxia condition. Escin is a potential therapeutic agent for clinical use in preventing the invasion of human malignant lung tumors.