Comprehensive Network Analysis Of The Molecular Regulation Mechanism For Breast Cancer Metastasis

Breast cancer is one of malignant severe diseases that cause cancer death in women. Although research about the pathogenesis and studies about treatment mechanisms in breast cancer have become clear focuses, we have no clear conclusion yet. Therefore, this research is based on a modular approach to explore key factors and molecular mechanisms that affect breast cancer metastasis. First of all, it is necessary to download breast cancer-related data on the GEO database, and we analyzed the difference between primary tumors and metastatic lesions to obtain differential gene expression profiles. On this basis, a series of bioinformatics analyses were performed to comprehensively, and they were presented to identify critical regulators in breast cancer metastasis. We have obtained a total of five co-expression modules, among which HECW1, FBN1, and other genes have effective regulation in dysfunction modules, and thus they would be recognized as driving genes for breast cancer metastasis. Module genes were significantly enriched in biological function, for instance, leukocyte-cell adhesion and negative regulation in the immune system process. At the same time, it substantially regulates signaling pathways, for example, fatty acid degradation, synthesis, and degradation of ketone bodies, and amino acid metabolism. Finally, we identified ncRNA pivots (including FENDRR, miR-19a-3p, and miR-26b-5p) and TF pivot (including NFKB1 and SP1) to regulate dysfunction modules significantly. Our study identified the coexpression network of genes involved in breast cancer metastasis. These results may be helpful to reveal the gene modules and regulatory factors of breast cancer. Importantly, we identified a long non-coding FENDRR that inhibits breast cancer metastasis through a fatty acid degradation signaling pathway, providing new directions and targets for subsequent studies.