Biomol Ther  
Anti-Proliferative Activities of Vasicinone on Lung Carcinoma Cells Mediated via Activation of Both Mitochondria-Dependent and Independent Pathways
Tapan Dey1,2, Prachurjya Dutta1,3, Prasenjit Manna1,3, Jatin Kalita1,3,*, Hari Prasanna Deka Boruah1,3, Alak Kumar Buragohain2 and Balagopalan Unni4
1Biological Sciences and Technology Division, CSIR-North East Institute of Science and Technology, Jorhat 785006,
2Centre for Biotechnology and Bioinformatics, Dibrugarh University, Dibrugarh 786004,
3Academy of Scientific and Innovative Research, CSIR-North East Institute of Science and Technology Campus, Jorhat 785006, Assam,
4Biological Sciences, Assam Downtown University, Guwahati 781026, India
E-mail: kalitajk74@gmail.com
Tel: +91-376-2370121, Fax: +91-376-2370011
Received: April 27, 2017; Revised: July 11, 2017; Accepted: August 14, 2017; Published online: January 9, 2018.
© The Korean Society of Applied Pharmacology. All rights reserved.

Abstract
Vasicinone, a quinazoline alkaloid from Adhatoda vasica Nees. is well known for its bronchodilator activity. However its anti-proliferative activities is yet to be elucidated. Here-in we investigated the anti-proliferative effect of vasicinone and its underlying mechanism against A549 lung carcinoma cells. The A549 cells upon treatment with various doses of vasicinone (10, 30, 50, 70 μM) for 72 h showed significant decrease in cell viability. Vasicinone treatment also showed DNA fragmentation, LDH leakage, and disruption of mitochondrial potential, and lower wound healing ability in A549 cells. The Annexin V/PI staining showed disrupted plasma membrane integrity and permeability of PI in treated cells. Moreover vasicinone treatment also lead to down regulation of Bcl-2, Fas death receptor and up regulation of PARP, BAD and cytochrome c, suggesting the anti-proliferative nature of vasicinone which mediated apoptosis through both Fas death receptors as well as Bcl-2 regulated signaling. Furthermore, our preliminary studies with vasicinone treatment also showed to lower the ROS levels in A549 cells and have potential free radical scavenging (DPPH, Hydroxyl) activity and ferric reducing power in cell free systems. Thus combining all, vasicinone may be used to develop a new therapeutic agent against oxidative stress induced lung cancer.
Keywords: Vasicinone, Antioxidant, Anti-proliferative, A549 cells


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