Acta Scientific Cancer Biology (ASCB) (ISSN: 2582-4473)

Review Article Volume 7 Issue 4

Attenuation of ROS Mediated Regulation of Cell Signaling by Bee Venom and Melittin in Cancer Progression

Monalisa Parija1,2 and Sandip K Mishra1*

1Cancer Biology Lab, Gene Function and Regulation Group, Institute of Life Sciences, Nalco Square, Chandrasekharpur, Bhubaneswar, India
2Regional Centre for Biotechnology, NCR Biotech Science Cluster, Haryana (NCR Delhi), India

*Corresponding Author: Sandip K Mishra, Cancer Biology Lab, Gene Function and Regulation Group, Institute of Life Sciences, Nalco Square, Chandrasekharpur, Bhubaneswar, India.

Received: May 03, 2023; Published: May 29, 2023

Abstract

Reactive oxygen species (ROS), a component of free radicals has emerged as a potential target that can elicit a cascade of cell cycle regulatory events to facilitate tumor progression. Recent reports suggest G-protein coupled receptors (GPCRs) mediated ROS activation promotes deregulated cellular signaling. Melittin, a bee venom product competently targets ROS-mediated signaling such as GPCR, mitogen-activated protein kinase (MAPK), and nuclear factor-κB (NF-κB) signaling pathways, which will eventually lead to regression in tumor development. Soaring interests toward natural anticancer drugs, Bee venom is on the bright side for future use in clinical practices when coupled with nanoparticles and other therapeutic agents. Melittin can further provide a potent system for better drug delivery to the targeted tumor. This review enlightens the efficacy of bee venom and melittin to hinder ROS-mediated tumor progression.

 Keywords: Reactive Oxygen Species; G Protein Coupled Receptors; Cell Signaling; Bee Venom; Melittin; Cancer

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Citation

Citation: Monalisa Parija and Sandip K Mishra. “Attenuation of ROS Mediated Regulation of Cell Signaling by Bee Venom and Melittin in Cancer Progression" Acta Scientific Cancer Biology 7.4 (2023): 03-11.

Copyright

Copyright: © 2023 Monalisa Parija and Sandip K Mishra. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.




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