Marsdeniae tenacissimae extract (MTE) has been used as an adjuvant medicine for cancer therapy for a long time. Although massive studies demonstrated its considerable anti-cancer effect, there is no research on its influence on erythrocytes, which are firstly interacted with MTE in the circulation. To investigate the influence of MTE on erythrocytes, we used a flow cytometer to detect the MTE-treated alternations of morphology, calcium concentration, and reactive oxygen species (ROS) level in erythrocytes. We used hemolysis under different osmotic solutions to evaluate the fragility of erythrocytes. Data showed that MTE treatment dose-dependently increased the ratio of erythrocyte fragmentation (P<0.001) and shrinking, and elevated the forward scatter (FSC) value (P<0.001) and calcium accumulation (P<0.001). MTE induced ROS production of erythrocytes under the high glucose condition (P<0.01) and consequently caused a rise in fragility (P<0.05). These results suggest that MTE induces cytotoxicity and aging in erythrocytes in a dose-dependent manner, and presents the possibility of impairment on cancer patients' circulating erythrocytes when MTE is used as an anti-cancer adjuvant medicine.

Background. Hepatocellular carcinoma (HCC) is a common tumor of the digestive system. Cell death is an essential process in normal tissue that consists of 3 classical pathways: apoptosis, necrosis and autophagy.Objectives. To perform a comprehensive analysis of the impact of cell death on liver cancer. Materials and methods.The Kyoto Encyclopedia of Genes and Genomes (KEGG) database and the Cancer Genome Atlas (TCGA) datasets were used to analyze the relationships between mutations in cell death-related genes and clinical variables of HCC. Then, we applied the DESeq2 package to identify aberrantly expressed genes in HCC and their related biological functions through a Pearson correlation analysis. Finally, a cell death-related signature of HCC was constructed using the single-factor Cox regression.Results. We identified the genes involved in apoptosis, necrosis and autophagy, of which TP53 and SPTA1 had the highest frequency of mutations. The results revealed that cell death-related tumor mutational burden (TMB) was significant for the pathologic stage and had a strong relationship with the prognosis. Moreover, 53 cell death-related genes that are differentially expressed in HCC were screened, and 3 of them were correlated with HCC prognosis. Harvey rat sarcoma viral oncogene homolog (HRAS) affected the infiltration of immune cells and was closely correlated with ferroptosis. Peptidylprolyl isomerase A (PPIA) played a significant role in mitochondrial pathways. At last, we constructed a cell death-related signature of HCC using 10 prognosis-related genes and a nomogram based on 3 variables (expression, group and stage).Conclusions. This study provided a comprehensive analysis of cell death-related genes in HCC based on multi-omics data, identified the contribution of each variable to clinical outcome and predicted the survival probability of HCC patients more directly.