Study the Effects of Capsaicin on Triple Negative Breast Cancer Cells

Abstract

Triple negative breast cancer (TNBC) is one of the most aggressive types of breast cancer accounting for 12% of breast cancer cases. It is characterized by the lack of the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER‐2), which limits treatment options and enhances its ability to metastasize with the risk of recurrence. Patients with TNBC are not responsive to conventional therapies. Capsaicin (CAP) is the most abundant capsaicinoid produced in chili pepper fruits and has been utilized for its analgesic and anti‐inflammatory effects. While several studies have demonstrated that capsaicin has anti‐carcinogenic properties in various types of human cancers, the underlying molecular mechanisms remain to be explored. The aim of this study was to investigate the effects of capsaicin in human TNBC, utilizing a BT‐20 cell model. Capsaicin demonstrated concentration‐ and time‐dependent in the viability of BT‐20 cells, as determined by the MTS assay. Capsaicin caused significant increases in cytochrome C release, caspase 3/7 activity and expression of cleaved poly‐(ADP‐ribose) polymerase (PARP), all of which are markers of apoptotic activation. These effects were accompanied by down‐regulation of cyclin D1 production, an indicator of cell cycle arrest at the G0/G1 phase. Further analyses of signaling mechanisms revealed that capsaicin significantly inhibited EGFR phosphorylation and the phosphorylation of its downstream signaling proteins AKT and MAPK, which may provide some explanation for its mechanism of action in TNBC. In conclusion, capsaicin has demonstrated inhibitory effects on cell growth and cell cycle progression on TNBC cells by enhancing apoptosis. Our data demonstrated a novel mechanism for capsaicin, modulating EGFR signaling by AKT/MAPK pathways in BT‐20 cells. These results provide useful information relevant to the development of a potential new therapy to treat TNBC with capsaicin.Support or Funding InformationThis work was funded by the College of Medicine, King Saud bin Abdulaziz University for Health Sciences (KSAU‐HS), Jeddah, Saudi Arabia.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.