Description:
Despite the tremendous progress in breast cancer diagnosis and treatment, the mortality rate is expected to increase due to the emergence of drug resistance. Pro-inflammatory markers are thought to contribute to drug resistance by activation of its naive receptors and its downstream signaling pathways. Elevation of pro-inflammatory markers leads to an increase in the biosynthesis of estrogen which can promote the proliferation of estrogen receptor (ER)+ breast cancer. Inflammation also results in obesity which is one of the key risk factors. Estrogen receptor-beta (ER-?) is an important target that has been widely studied and accepted to possess anti-cancer activity in a number of cancers including breast cancer. ER-? elicits its action through genomic and non-genomic pathways. The genomic pathway increases the transcription of potent cyclin-dependent kinase inhibitor (p21), and tumor suppressor genes such as melanoma differentiation associated gene 7 and tumor protein (p53). The non-genomic pathway works through protein-protein interaction and phosphorylation. Here, we propose that the activation of ER-? might enhance the activation of nuclear factor-erythroid factor 2-related factor 2 (Nrf2) via estrogen receptor-alpha (ER-?) repression. The activation of Nrf2 increases the transcription of antioxidant genes such as NADH quinone oxidoreductase 1 (NQO1), heme oxygenase-1 (HO1), etc., and decreases the expression of pro-inflammatory genes such as tumor necrosis factor-? (TNF-?), interleukin-1 (IL-1), etc. This review hypothesizes and suggests that ER-? agonists could play a beneficial role to overcome inflammation-related drug resistance by modulation of the Nrf2/antioxidant response element (Nrf2/ARE) pathway

URL:
http://103.158.96.210:88/web_repository/uploads/no_data.jpg

Type:
Journal

Document:
Diploma III Farmasi

Date:
23-06-2024

Author:
Emdormi Rymbai