Breast cancer, which is the most common type of cancer in women, is the second leading cause of cancer-related death in women [13]. Research regarding the role of dysregulated cell turnover in breast cancer has led to the emergence of therapeutically important targets [4, 5]. Therefore, various antioxidants have been used in research on breast cancer. In a study done, it was reported that quercetin induced apoptosis in MCF7 breast cancer cell lines [14]. In another study, it was reported that resveratrol inhibited metastasis and migration in MDA-MB-231 breast cancer cells [15]. In addition, researchers have demonstrated the apoptotic effects of curcumin in studies on breast cancer cells [16, 17].
The key protein in ERS is glucose regulatory protein 78 [18]. Although many studies have focused on breast cancer tissues and breast cancer cells in vitro, the mechanisms regulating ERS-induced apoptosis have not yet been fully elucidated. Studies related to ERS have been performed in breast cancer cells [19, 20]. Rachakhom et al., in their study on MCF7 and MDA-MB-231 cell lines, reported that a dihydrocalone derivative from flavonoid varieties stimulated apoptosis in breast cancer cell lines by stimulating the ERS pathway and activating pro-apoptotic pathways [21]. In a similar study, Ghosh et al. showed that Vitaferin A, which has an antitumoral effect in MCF-7 and MDA-MB-231 breast cancer cell lines, caused an increase in the expression of GRP78 and CHOP proteins, which are chaperone proteins associated with ERS stress, resulting in apoptosis of breast cancer cells [22].
Flavopiridol, a potent inhibitor of CDKs, has antitumor activity against various types of cancer. Li et al. reported in their study that flavopiridol also caused apoptosis in DU145 prostate cancer cells. In their studies, they reported that the substance applied at a dose of 400 nM was the most effective dose and also stopped the cell cycle at the G0/G1 phase [23]. Cimini et al. showed that flavopiridol administered on the U87 glioblastoma cell line significantly reduced cell viability at a dose of 492 nM for 24 hours [24]. In another study, they reported that flavopiridol in KKU-055 and KKu-213 colon cancer cell lines with the Annexin V experiment, 300 nM dose for 24 hours was an effective dose at the apoptotic rate and stopped the cell cycle in the G2/M phase [25]. Shao et al. showed that flavopiridol stopped the cell cycle in the G1 phase and also stimulated apoptosis in MCF7 breast cancer cell lines [26]. Wang S et al. reported that flavopiridol was the most effective dose for cell viability in MCF-7 breast cancer cell line, especially at a dose of 1 µM for 24 hours [27]. Studies with breast cancer and flavopiridol are very few. Looking at the studies done so far, there is no study with flavopiridol on ERS and ERS-related apoptosis pathway in breast cancer cells. In this study, we found that flavopiridol was significantly effective on breast cancer cells. More studies are needed as no studies have been conducted on the ERS pathway of flavopiridol on breast cancer so far.