On the other hand, we observed 7 miRs of which miR-98, miR-486-3p, and miR-874 showed low values of co-expression correlation and miR-124, miR-381, miR-501-5p, and miR-660 showed high values of coexpression correlation in F-BC compared with NF-BC network profile. Out of 49, 8 not predicted miR–mRNA interactions showing inverse correlation could also distinguish F-BC from NF-BC tumors. Among them 5 pairs could be considered as predicted targets albeit using less stringent criteria. From 49 miR–mRNA interactions, 24 showed differentially expressed genes and significant coexpression differences; however, they did not exhibit inverse signal of fold-change value, suggesting that the separation between F-BC from NF-BC tumors could not be exclusively explained by the predominant mechanism of miRs-mediated gene repression. We perBortezomib formed functional analysis using the IPA program on a set formed by 28 unique genes representing 49 predicted/not predicted miRmRNA interactions listed in table S4. The results from functional analysis demonstrated over representation of some biological processes involved with: apoptosis, cell death, and fibroblast proliferation. We present the results of integrated analysis of miR/mRNA data from the same tumor tissue samples to identify genes that could differentiate between tumor harvested from young patients with familial BC and those from sporadic BC, not harboring BRCA1/BRCA2 mutations. We identified a set of 9 miRs whose expression levels, rather than miR identity, were able to correctly separate, with high accuracy, familial and non-familial young BC patients. A subset of these miRs has previously been characterized as BC regulatory genes, including miR-486-3p, miR-98, miR-874, miR-210, miR-124, whereas miR-660 has been associated with other cancers or tissue types. We next identified a set of miRs showing significant negative or positive correlations with those of their targets. Approximately 34,6% retained inversely correlated miR–mRNA interactions. An interaction network revealed changes in the co-expression of these miR-mRNA pairs that were able to distinguish familial from sporadic breast cancer. For instance, a decreased expression of miR-874, miR-98 and miR-486-3p were associated with increased expression of their predicted target genes in F-BC cases. MiR-874, which has been previously associated with unfavorable prognosis in invasive breast cancer was inversely correlated with several of their paired genes, suggesting that miR-874 has a critical role in the regulation of genes preferentially expressed in F-BC. This analysis revealed genes involved in embryonic stem cell self-renewal, such as STAT3 and EZH1. FGD6 is a mediator of EGFR endocytosis and its inhibition in BC coincided with an enhanced EGF-signaling. TBRG1 was previously identified as one of the TGFb1-responsive genes and has been described as a novel growth inhibitor that contributes to the maintenance of chromosomal stability. VPS13A codes for vacuolar sorting proteins, and its loss was observed in colorectal and gastric cancers with high microsatellite instability.