Association Between Depression and Breast Cancer: TNF/TNFRSF1β and LEP/LEPR Axis
Abstract Depression contributes to enhanced initiation, development and metastasis of breast cancer. Despite epidemiological studies and experimental data suggest that depression and breast cancer may share a common biological mechanism, the results from these studies remain inconsistent. Here, we fully focus on the underlying biological mechanism behind the adverse effects of depression against breast cancer patients, and highlight the practical therapeutic intervention and improving quality of life. Publicly available datasets deposited in the Gene Expression Omnibus (GEO) were downloaded. Gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses of the differentially expressed genes (DEGs), which were extracted by using R tools, were performed. The protein-protein interaction network of the target DEGs was constructed using Cytoscape software and the hub genes were identified. In our study, we found that genes encoding proinflammatory cytokine, such as IL-1β and TNF, had significantly increased expression in depression. Following chronically stimulated by TNFα and IL-1β (usually for 14-18 days), inflammatory cancer-associated fibroblasts (CAFs) had elevated expression of inflammatory genes. Furthermore, the TNF/TNFRSF1β and LEP/LEPR regulatory axes were proven to be hub pathways of the crosstalk between depression and breast cancer. Our findings demonstrate that inflammatory factors are messengers linking depression and breast cancer, and provided further guidance in clinical medication.