Enriched in flavonoid compounds, phenol acids, and terpene derivatives, propolis has been shown to regulate apoptosis signaling pathways and alter the expression of microRNAs (miRNAs). In the present study, it has been aimed to examine the effects of Turkish propolis on miRNA levels of breast cancer (MCF-7) cells, and its relationship with cell proliferation and apoptosis. Cytotoxic activity of ethanolic propolis extract (EEP) was evaluated using MTT assay. Mechanisms involved in the cytotoxic action of Turkish propolis in MCF-7 cells were investigated with regard to apoptosis and cell cycle using flow cytometry and western blot. Mitochondrial membrane potential (MMP) were evaluated by spectrofluorometric method. miRNA levels were detected by qRT-PCR method. EEP exhibited selective toxicity against MCF-7 cells compared to normal fibroblast cells. EEP increased the cell cycle arrest at the G₁ phase. EEP elevated the apoptotic cell death through increasing pro-apoptotic protein levels (p21, Bax, p53, p53-Ser46, and p53-Ser15), decreasing MMP and altering the expression levels of specific tumor suppressors (miR-34, miR-15a, and miR-16-5p) and oncogenic (miR-21) miRNAs. These data support that Turkish propolis may be evaluated as a potential natural agent for new anticancer drugs in future.

Breast cancer (BC) is the most common heterogeneous disease in women and one of the leading causes of cancer-related death. Surgery, chemotherapy, radiotherapy, hormone, and targeted therapy are the gold standards for BC treatment. One of the significant challenges during the treatment of BC represents resistance to chemotherapeutics, resistance that severely limits the use and effectiveness of the drugs used for BC treatment. Therefore, it is essential to develop new strategies to improve therapeutic efficacy. Circular RNAs (circRNAs) are a large group of non-coding RNAs that covalently form closed circular loops by joining their 5′, and 3′; ends. Accumulating evidence suggests that circRNAs have a vital role in cancer development, progression, and BC resistance to chemotherapy. The purpose of this review is to discuss the biological properties of circRNAs, and how circRNAs induce resistance to conventional therapeutic anti-cancer drugs used in BC treatment, by emphasizing and summarizing the potential roles of circRNAs in mechanisms of drug resistance, such as drug efflux, apoptosis dysfunction, autophagy, and DNA damage repair. CircRNAs are associated with drug resistance via ATP-binding cassette (ABC) efflux transporters, while some others by inhibition of cell apoptosis, thus leading to resistance to tamoxifen in BC cells. In contrast, others are involved in the promotion of BC cells chemoresistance by doxorubicininduced autophagy. CircRNAs may have clinical significance in regulating or overcoming BC drug resistance and may give directions towards a novel approach to personalized BC treatment. CircRNAs may significantly contribute to the identification of new therapeutic targets for the prevention of BC chemoresistance.

In patients with endometriosis, ectopic endometrial tissues can escape from immune system control and survive in other tissues. The pathophysiology of endometriosis is still not fully understood. In this study, we aimed to clarify the pathophysiology of endometriosis, which is thought to be a benign but infiltrative cancer type, which has many similarities with cancer biology by determining PD-1 expression in patients with endometriosis. In this study, n = 73 cases who underwent surgery or examination at the Obstetrics and Gynecology Clinic of Sivas Cumhuriyet University Faculty of Medicine and diagnosed as endometriosis in the biopsy material taken with the pre-diagnosis of endometriosis constituted the patient group. The control group consisted of n = 64 healthy subjects without concomitant malignancy or chronic inflammatory disease. Venous whole blood samples were obtained from the study groups. PD-1 and PD-L1 levels were determined by the ELISA method from serum and plasma samples. PD-1 gene expression level was determined by RT-PCR. The PD-1 level was found to be approximately 350 +/- 150 ng/L and 45 +/- 17 ng/L in endometriosis and control group, respectively. While the PD-L1 level was approximately 760 +/- 108 ng/L in the patients, this level was 140 +/- 14 ng/L in the controls. According to the RT-PCR results, the expression of the PD-1 gene 10 times higher compared to the controls. Conclusion: The identified increase of PD-1 levels and gene expression in endometriosis groups show that immunotherapy may be used in the treatment of endometriosis.