CHANGES IN THE KEAP1-NRF2-ARE PATHWAY AS A CHEMORESISTANCE TRIGGERING FACTOR AND AGGRESSIVE TUMORIGENIC ACTIVITY IN OVARIAN CARCINOMA

International Journal of Development Research

Volume: 
13
Article ID: 
27396
5 pages
Research Article

CHANGES IN THE KEAP1-NRF2-ARE PATHWAY AS A CHEMORESISTANCE TRIGGERING FACTOR AND AGGRESSIVE TUMORIGENIC ACTIVITY IN OVARIAN CARCINOMA

João Gabriel Pimentel Soares; Eduardo de Sousa Lucena; Rodrigo Cruz de Carvalho and Luan Kelves Miranda de Souza

Abstract: 

Introduction: Cancer is understood as the term used to agglutinate the more than 100 types of malignant diseases that have as a common characteristic the disordered growth of cells, which can invade adjacent tissues or organs at a distance. There are many risk factors associated with a proliferation of neoplastic cells, and the Keap1-Nrf2-ARE signaling pathway (Kelch-like ECH-associated protein 1 - Nuclear factor- erythroid-2 related factor 2 - Antioxidant response element) is one of the main cellular sensors of oxidative stress, a factor that fits within the extensive list of genetic propensity to the appearance. Objective: To understand the KEAP1- NRF2-ARE pathway and analyze chemoresistance factors in the formation of ovarian tumors. Methodology: This is an integrative review of the literature, which uses an exploratory and descriptive methodology. Initially, studies were searched in the electronic databases: Latin American and Caribbean Literature in Health Sciences (Lilacs); Scientific Electronic Library Online (SciELO); Medical Literature Analysis and Retrieval System Online (Medline) and National Library of Medicine (PubMed). For research of such articles, the following descriptors were used: Ovarian carcinoma; Chemoresistance; KEAP1- NRF2-ARE. In the cataloging of these studies we used the Boolean operator "AND" in the descriptors of the health sciences (DECS). Results: The role of the KEAP1-NRF2-ARE pathway in the process of controlling cellular oxidative stress was understood, as well as its relevance in the treatment of ovarian neoplasms. Furthermore, the functioning of this mechanism was also understood and how its protective mechanism becomes favorable in the development and proliferation of neoplastic cells. Confirming that the study has full potential to serve as a vehicle for promoting scientific-based studies, as well as the implementation of evidence-based medicine. Making it of great value for understanding and studying effective therapies in the oncological scope of ovarian neoplasms.

DOI: 
https://doi.org/10.37118/ijdr.27396.11.2023
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