Breast cancer is one of the most common causes of deaths worldwide. Major obstacles to treatment have contributed to the increasing popularity of complementary or alternative therapies. Although recent results support the mechanism that honey induces cell death, the full mechanisms are still unknown. This study investigates the potential use of Pervari honey (PH) as an in vitro therapeutic agent in breast cancer. Firstly, the antioxidant capacity and total phenolic content of PH were tested. In addition, MCF-7 and MDA-MB-231 breast cancer cells treated with PH were examined for cell viability, reactive oxygen species production, oxidative deoxyribonucleic acid (DNA) damage, and apoptosis. Our results show that PH treatment decreased cell viability dose-dependently and increased reactive oxygen species (ROS) levels, oxidative DNA damage, and apoptosis rate. The present study suggests that honey is a promising source to produce pharmaceuticals and nutraceuticals for breast cancer therapy.

Paracetamol (acetaminophen) is a widely used analgesic and antipyretic drug. Although many studies are available showing that paracetamol causes hepatic damage, few studies exist on renal damage. Protein tyrosine phosphatase receptor type O (PTPRO) protein has tyrosine phosphatase activity and plays a role in the regulation of the renal glomerular pressure/filtration rate relationship in podocyte structure. The PTPRO gene also exhibits characteristics of a candidate tumor suppressor gene. In this study, apoptosis, cell cycle, colony formation, and PTPRO gene expression of the human embryonic kidney (HEK 293) cells were assessed by treating with paracetamol at different concentrations for 24 and 26 h in at least three independent trials. Paracetamol induced dose‐dependent apoptosis at all concentrations (5, 10, 15, 20, and 30 mM) for both 24 and 26 h ( p < 0.05– p < 0.001). Paracetamol decreased dose‐dependent colony‐forming potential of cells at 10.000 cells seeding in HEK 293 cells at all concentrations (5, 10, 15, 20, and 30 mM) ( p < 0.05– p < 0.001). In HEK 293 cells, paracetamol also increased cell population in the G0‐G1 phase at low 5 mM concentration for 26 h ( p < 0.05), while reducing cell population in the G2‐M phase of the cell cycle at 10 mM and increasing at 30 mM concentration for 24 h ( p < 0.05 and p < 0.05, respectively). Paracetamol at high concentration (30 mM) increased PTPRO gene expression in HEK 293 cells for both 24 and 26 h ( p < 0.05). In conclusion, our results may indicate that paracetamol may suppress the development of renal cancer by inducing apoptosis and reducing colony formation in a dose‐dependent manner, and upregulating PTPRO gene expression in HEK 293 cells at high concentration, in addition to its renal‐damaging role. Further research is necessary to determine the potential role or detrimental effects of paracetamol on the development of renal cancer, as the mechanism underlying its effects on renal damage and cancer formation remains unclear.

Background: Gaucher disease (GD) occurs due to a mutation in the glucosylcerami-dase (GBA) gene and is a common lysosomal storage disease. It is well known that there is a strong association between the abnormal expression of miRNAs and various diseases including cancer. These abnormally expressed miRNAs can be used as biomarkers. Interestingly, several studies have reported a linkage between GD with an increased risk of cancer. Therefore, in the current study, we investigated the expression levels of selected miRNAs that are associated with cancers that might have potential use as biomarkers in GD. Methods: Blood samples were collected from 24 healthy volunteers, 6 carriers, and 20 treated patients with type 1 GD. A reverse transcription-quantitative real-time PCR (RT-qPCR) platform was used to analyze the miRNA expression levels. Results: While carriers had lower relative expressions of miRNA-15a with tumor suppressor ef-fect, and miRNA-150 and miRNA-181b with oncogene effect, treated patients with type 1 GD had lower relative expressions of miRNA-15a and miRNA-125b with tumor suppressor effect and higher relative expression miRNA-21 with oncogene effect (p<0.001, p<0.05, p<0.01, p<0.05, p<0.001, and p<0.05, respectively). Conclusion: The results suggested that the downregulation of miRNA-15a and miRNA-125b expressions with tumor suppressor effect and the upregulation of miRNA-21 expression with on-cogene effect can be indicated to an increased risk for cancers such as multiple myeloma (MM), B-cell lymphoma, leukemia, and hepatocellular carcinoma (HCC) in GD.