Background. Du Zhong (DZ), or Eucommiae Cortex, a traditional Chinese herbal medicine, has been used to treat osteoporosis. Although it has been reported that DZ can improve bone mass in ovariectomized rats, its pharmacological mechanisms in treating osteoporotic fractures (OPF) remain unclear. Methods. In this study, we used a network pharmacological manner to explore its potential complicated mechanism in treating OPF. We obtained DZ compounds from TCMSP and BATMAN-TCM databases and collected potential targets of these compounds through target fishing based on TCMSP and BATMAN-TCM databases. Next, we collected the OPF targets by using CTD, GeneCards, OMIM, HPO, and GenCLiP 3 databases. And then the overlapping genes between DZ potential targets and OPF targets were used to build up the protein-protein interaction (PPI) network and to analyze their interactions and find out the big hub genes in this network. Subsequently, clusterProfiler package in R language was utilized to conduct the enrichment of Gene Ontology biological process and KEGG pathways. Results. There were totally 93 active compounds and 916 related targets in DZ. After the enrichment analysis, we collected top 25 cellular biological processes and top 25 pathways based on the adjusted P value and found that the DZ anti-OPF effect was mainly associated with the regulation of ROS and inflammatory response. Furthermore, 64 hub genes in PPI network, such as MAPK1 (degree = 41), SRC (degree = 39), PIK3R1 (degree = 36), VEGFA (degree = 31), TP53 (degree = 29), EGFR (degree = 29), JUN (degree = 29), AGT (degree = 29), MAPK1, SRC, PIK3R1, VEGFA, and TP53, were considered as potential therapeutic targets, implying the underlying mechanisms of DZ acting on OPF. Conclusion. We investigated the possible therapeutic mechanisms of DZ from a systemic perspective. These key targets and pathways provided promising directions for the future research to reveal the exact regulating mechanisms of DZ in treating OPF.
Background: Pancreatic adenocarcinoma(PAAD) is a digestive solid tumor with a poor prognosis among many common cancers. Now a new way of cell death has been discovered. This mode of death is known as disulfide death and may be associated with tumor progression. However, the role of this gene in PAAD and its relationship to prognosis remains unclear. This study aims to explore the prognostic role of disulfide death-related genes in breast cancer and their effects on immunity and interstitium. Result: In this study, PAAD samples from TCGA, GTEx, and GEO databases were used to investigate the expression of 10 disulfide death-related genes and the predictive potential of patients' prognosis and survival. Univariate Cox regression analysis was used to analyze 10 genes, and it was found that NCKAP1 and RPN1 were highly expressed in pancreatic cancer tissues and correlated with the overall survival of patients. Univariate and multivariate Cox regression analysis showed that NCKAP1 was an independent factor affecting the prognosis of patients. This study combined NCKAP1 with some clinical factors to construct an ideal prognostic model. In addition, in our study, NCKAP1 was found to be closely related to cancer immune response, and significantly correlated T-cell infiltration, chemotherapy drug sensitivity, and sulfur metabolic channels. The difference in the expression level of NCKAP1 in pancreatic cancer cells and normal controls was verified by the GEO cohort, which was consistent with the public database TCGA. Conclusion: NCLAP1 may play a role in inducing disulfdptosis and regulating tumor immunity, and can serve as a potential therapeutic target for PAAD.
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