Background Liver cancer is the sixth most commonly diagnosed cancer and the fourth most common cause of cancer death. The purpose of this work is to find new diagnostic biomarkers or prognostic biomarkers and explore the biological functions related to the prognosis of liver cancer. Methods GSE25097 datasets were firstly obtained and compared with TCGA LICA datasets and an analysis of the overlapping differentially expressed genes (DEGs) was conducted. Cytoscape was used to screen out the Hub Genes among the DEGs. ROC curve analysis was used to screen the Hub Genes to determine the genes that could be used as diagnostic biomarkers. Kaplan-Meier analysis and Cox proportional hazards model screened genes associated with prognosis biomarkers, and further Gene Set Enrichment Analysis was performed on the prognosis genes to explore the mechanism affecting the survival and prognosis of liver cancer patients. Results 790 DEGs and 2162 DEGs were obtained respectively from the GSE25097 and TCGA LIHC data sets, and 102 Common DEGs were identified by overlapping the two DEGs. Further screening identified 22 Hub Genes from 102 Common DEGs. ROC and survival curves were used to analyze these 22 Hub Genes and it was found that there were 16 genes with a value of AUC > 90%. Among these, the expression levels of ESR1,SPP1 and FOSB genes were closely related to the survival time of liver cancer patients. Three common pathways of ESR1, FOBS and SPP1 genes were identified along with seven common pathways of ESR1 and SPP1 genes and four common pathways of ESR1 and FOSB genes. Conclusions SPP1, AURKA, NUSAP1, TOP2A, UBE2C, AFP, GMNN, PTTG1, RRM2, SPARCL1, CXCL12, FOS, DCN, SOCS3, FOSB and PCK1 can be used as diagnostic biomarkers for liver cancer, among which FOBS and SPP1 genes can also be used as prognostic biomarkers. Activation of the cell cycle-related pathway, pancreas beta cells pathway, and the estrogen signaling pathway, while on the other hand inhibition of the hallmark heme metabolism pathway, hallmark coagulation pathway, and the fat metabolism pathway may promote prognosis in liver cancer patients.

As research was conducted on the early apoptosis of human breast cancer cell MCF-7 caused by lycorine hydrochloride and the expression of the related apoptosis proteins. The early-period apoptosis rate of human breast cancer cell MCF-7 was tested with the AnnexinV/PI double staining and flow cytometry. The Western Blotting method was also used to detect the protein expression conditions of Fas, FasL, Caspase-8 and Bid. The results showed that the higher the dose, the higher the rate of apoptosis and that the rate of apoptosis was dependent on the dose; the relative protein activity of Fas, FasL, Caspase-8 and bid gradually rose with the increase of lycorine dosage and the activities revealed certain dose-independence. Results showed that lycorine hydrochloride could induce the apoptosis of human breast cancer cell MCF-7 through the death receptor pathway.

In this study, ultrasound-assisted extraction of flavonoid from Crinum asiaticum was studied through response surface methodology (RSM) to gain the best extraction process of flavonoid and enhance the extraction rate of flavonoid. In the following RSM experiment, we selected the corresponding data of every factor as the center point through the single-factor experiments, then the experimental data was subjected to multiple regression analysis. According to the statistical analysis results, the results were consistent with the polynomial regression model, the determination coefficient (R2) was 0.9769. The best conditions for maximum flavonoid yield were 60% ethanol concentration, 64 °C for extraction temperature, 1:28 (v/w) solid-to-liquid ratio with extraction time for 47 min. The best response of flavonoid yield was 1.63972%. The predicted results for best reaction conditions were in good agreement with experiment values. Ultrasound-assisted extraction method can enhance the extraction rate of flavonoid significantly. It is a powerful tool to extract of important phytochemicals from nature plant.

ABSTRACT. This study investigated the nature and mechanism of juglone-induced apoptosis in the human breast cancer cell line MCF-7. The inhibitory effect of juglone on MCF-7 cell growth was evaluated by the dimethylthiazol tetrazolium assay. Morphological apoptotic changes were characterized using an inverted microscope, Hoechst 33258 fluorescence staining, and Giemsa staining. The rate of cell apoptosis, intracellular levels of reactive oxygen species (ROS), and mitochondrial membrane potential were detected using flow cytometry. Intracellular Ca 2+ concentrations were detected using laser scanning confocal fluorescence microscopy. Expression of the proteins Bcl-2, Bax, and cytochrome C was assessed by western blotting. Caspase-3 activity was quantified using a caspase-3 activity kit. Juglone inhibited the growth of MCF-7 cell line with an IC50 of 11.99 µM. The rates of MCF-7 cell apoptosis at 24 h after exposure to 5, 10, and 20 µM juglone were 9.29, 20.67, and 28.39%, respectively; compared to unexposed cells, juglone-exposed cells exhibited significant elevation in intracellular ROS level, decrease in mitochondrial membrane potential, and increase in intracellular Ca 2+ concentration. Juglone upregulated the expression of Bax, and downregulated the expression of Bcl-2, promoting the release of cytochrome C, thereby upregulating the activity of caspase-3. The results suggest that the mechanism of juglone-induced apoptosis in MCF-7 cells is characterized by elevated ROS levels, reduced Bcl-2 expression, increased Bax expression, decreased mitochondrial membrane potential, increased intracellular Ca 2+ concentration, outer mitochondrial-membrane rupture, cytochrome C release, and caspase-3 activation.