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Introduction: Breast cancer is one of the most common malignancies in women. Treatment with herbal drugs has been considered by researchers due to the lower side effects. Curcumin is a polyphenol extracted from turmeric with confirmed anti-cancer properties. Curcumin is water-insoluble with rapid metabolism. Drug delivery using nano-carriers is suggested to overcome such limitations. The aim of this study was based on evaluating the effect of Dendrosomes curcumin on expression level of HOTAIR long noncoding RNA in MCF-7 breast cancer cell line. Methods: This study was an applied basic research. Firstly, curcumin was loaded in dendrosomes and the entry of dendrosomal curcumin into cells was studied using fluorescent microscopy. Cell death was investigated using MTT assay and apoptosis detection kit. The expression of HOTAIR gene was measured using real-time PCR. Increased expression of this gene was reported in a wide range of tumors. The data were analyzed using GraphPad Prism V9.5 statistical software, using NOVA one-way statistical analysis and Student t-test; the results were reported as mean ± standard deviation. Results: Dendrosomes increased the solubility of curcumin. The effective inhibitory doses of dendrosomal curcumin after 24 and 48h treatment were 25 and 20 micromolar, respectively. The percent of cells undergoing early apoptosis were 22.97±0.03 and 56.22±0.05, respectively, which was statistically significant in comparison with non-treated control cells. Following 24 and 48h treatment with 20 micromolar of dendrosomal curcumin, the HOTAIR gene expression was significantly decreased (P=0.001). Conclusion: These findings suggest that dendrosomal curcumin may promote breast tumor cells toward programmed cell death by reducing HOTAIR gene expression.

Background and purpose: Hyperlipidemia is one of the main risk factors for coronary artery disease and is defined as abnormal elevation of lipids or lipoproteins in the blood. Pcsk9 is the ninth member of the proprotein convertase family that binds to the LDLR on the surface of the hepatocyte, leading to degradation of LDLR in lysosomes which could cause hyperlipidemia. The present study aimed to analyze the methylation status of pcsk9 promoter in patients with hyperlipidemia. Materials and methods: This case-control study was conducted in 50 patients with hyperlipidemia and 50 healthy controls. DNA isolation from whole blood was performed using salting out procedure. Promoter methylation of the Pcsk9 gene was analyzed by methylation-specific PCR (MSP). Ten MSP products were sequenced to confirm the data obtained. Results: According to MSP results, methylation pattern of pcsk9 gene promoter displayed an unmethylated status among the patients and control individuals. In other words, no methylation was seen in case and control samples. Conclusion: The current study showed no significant association between PCSK9 methylation pattern and blood lipid profile level in case group and control group.