ERα and AhR mediated genomic effects of karanjin in breast cancer cells

Abstract

Karanjin, a bioactive flavonoid found in Pongamia pinnata seed oil, possesses a wide range of therapeutic properties, including antioxidant, antibacterial, anti-cancer, anti-ulcer, antihyperglycemic, and anti-inflammatory effects. In vitro, it has demonstrated potential as an anticancer agent by inhibiting cancer cell growth and promoting apoptosis. However, its effects on cell proliferation appear to be dose-dependent, with lower concentrations promoting proliferation and higher concentrations inhibiting it, particularly in breast cancer cells. The global transcriptomic footprint of MCF-7 and T47D breast cancer cells, suggests partial estrogen-like nature. Karanjin interacts with the estrogen receptor alpha (ERα), influencing gene expression and protein turnover. Interestingly, karanjin is postulated to be a novel phytoestrogen or SERM based on molecular and cellular effects produced on breast cancer cells. Additionally, it has been identified as a novel agonist of the aryl hydrocarbon receptor (AhR), similar to dioxin but without toxic effects. This research employs both in vitro and in silico methods to better understand how Karanjin regulates ERα and AhR, providing insights into its therapeutic potential.