The underlying molecular mechanism and drugs for treatment in adrenal cortical carcinoma

Abstract

The study aimed to predict and explore the possible clinical value and mechanism of genetic markers in adrenal cortical carcinoma using a bioinformatics analysis method. Methods: The RNA-seqs and miRNAs data were downloaded from TCGA database to identify the differentially expressed genes and differentially expressed miRNAs. The hub-genes were screened by building protein-protein interaction sub-networks with 12 topological analysis methods. We conducted the receiver operating characteristic curve to elevate the diagnostic value of hub-genes in distinguishing the death and alive groups. The survival analysis of hub-genes and key miRNAs were conducted using Kaplan-Meier curves. Furthermore, most significant small molecules were identified as therapeutic candidates for adrenal cortical carcinoma by the CMap analysis. Results: Compared to survival group, we found 475 up-regulated genes and 354 genes and the key pathways leading to the death of different ACC individual patients. Then we used 12 topological analysis methods to found the most possible 22 hub-genes. Among these hub-genes, nine hub-genes (C3, CXCL5, CX3CR1, GRM8, HCAR2, HTR1B, SUCNR1, PTGER3 and SSTR1) could be used to distinguish the death and survival groups for patients. We also revealed that mRNA expressions of 12 genes (C3,

Analysis of the role of m6A and lncRNAs in prognosis and immunotherapy of hepatocellular carcinoma

“…Axitinib combined with radiotherapy for advanced HCC was well tolerated, with ORR of 66.7%, 1-year OS of 66.7%, and median PFS of 7.4 months [ 86 ]. AZ628 was a hydrophobic Raf-kinase inhibitor that may play a therapeutic role in breast cancer [ 87 ], adrenocortical carcinoma [ 88 ]. Saracatinib (AZD.0530) treatment abolished the activation of Fyn, down-regulated the Fyn/FAK/N-WASP signaling pathway in hepatic stellate cells, and significantly reduced the degree of CCl4-induced liver fibrosis in mice [ 89 ].…”