Plant extracts are increasingly tested for their biological activity and interactions with neoplastic cells. One of such sources of biologically active substances is propolis. This product has been known for thousands of years and is widely used in alternative, folk medicine. Articles describing its effects on the metabolism and cell signaling pathways of neoplastic cells derived from different organs are also published more and more frequently. The purpose of our study was to evaluate the biological activity of propolis extract produced with the cold separation method into hormone-dependent and hormone-independent prostate cancer cell lines. In our study, the propolis extracts showed at least an inhibitory effect on the growth of PC-3 and DU-145 neoplastic cells. Our results suggest that propolis extracts obtained with the cold separation method may be considered as promising compounds for the production of health-promoting supplements.

Propolis and its extracts show a wide spectrum of biological activity. Due to the necessity to use high temperatures and high polarity in the eluent, the obtained extracts are depleted of active compounds. The new, cold separation method allows obtaining a qualitatively better product containing a number of chemical compounds absent in extracts obtained using high-temperature methods. The purpose of our study was to evaluate the biological activity of propolis extracts produced with the cold separation method in four female breast cancer cell lines: MDA-MB-231, MDA-MB-468, MCF-7, and T-47D. The results of the breast cancer cell viability were obtained using the MTT test. Propolis extracts at 75 and 80% showed similar cytotoxicity against cancer cells, with the polyphenol fraction 75% being slightly more negative for cells. Propolis extracts at concentrations of 50, 75, and 100 µg/mL significantly reduced cell viability. With the exception of the MDA-MB-231 line, cell viability was also decreased after incubation with a concentration of 25 µg/mL. Our results suggest that propolis extracts obtained with the cold separation method may be considered as promising compounds for the production of health-promoting supplements.

Leflunomide, an anti-inflammatory agent, has been shown to be effective in multiple myeloma (MM) treatment; however, the mechanism of this phenomenon has not been fully elucidated. The aim of the study was to assess the role of mitochondria and dihydroorotate dehydrogenase (DHODH) inhibition in the cytotoxicity of leflunomide in relation to the MM cell line RPMI 8226. The cytotoxic effect of teriflunomide—an active metabolite of leflunomide—was determined using MTT assay, apoptosis detection, and cell cycle analysis. To evaluate DHODH-dependent toxicity, the cultures treated with teriflunomide were supplemented with uridine. Additionally, the level of cellular thiols as oxidative stress symptom was measured as well as mitochondrial membrane potential and protein tyrosine kinases (PTK) activity. The localization of the compound in cell compartments was examined using HPLC method. Teriflunomide cytotoxicity was not abolished in uridine presence. Observed apoptosis occurred in a mitochondria-independent manner, there was also no decrease in cellular thiols level. Teriflunomide arrested cell cycle in the G2/M phase which is not typical for DHODH deficiency. PTK activity was decreased only at the highest drug concentration. Interestingly, teriflunomide was not detected in the mitochondria. The aforementioned results indicate DHODH- and mitochondria-independent mechanism of leflunomide toxicity against RPMI 8226 cell line.