ILs that stimulates T cell proliferation and activation. TRIMM44 is a member of tripartite motifcontaining protein family, which is an important regulator of carcinogenesis. Contrariwise, upregulated miRs in familial versus sporadic cases were correlated with a reduced expression of their target genes, including CA5B, ZNF480, SLC2A4RG, NUP35, NDFIP2, and FKBP4. FKBP4, a binding protein of SSEA-4 is a syalyl-glycolipid that has been commonly used as a pluripotent human embryonic stem cell marker. The inhibition of FKBP4 could reduce the expression of SSEA-4. SLC2A4R6 is associated with the recruitment of glut4 to the plasma membrane and its downregulation may decrease glucose uptake and AKT signaling. CA5B is an enzyme localized in the mitochondrial matrix that converts the CO2 produced by the TCA cycle to HCO32, which in turn controls metabolic pathways that increase oxidative phosphorylation. A decrease in CA5B levels may lead to a drop in intracellular pH and an activation of the pro-apoptotic protein BAX. Thus, gene profiling in familial BC appears to be associated with some biological Ruxolitinib processes that seem to characterize a less aggressive behavior compared to the sporadic cases. Our findings of coordinated expressed pairs between miR and mRNA predicted levels indicated that some miRs, including miR-501-5p, miR-660, miR-874, miR-98, miR-124, and miR-455-3p, act as positive regulators of their target mRNAs. The targets of this population appear to include mainly mRNAs associated with the embryonic development or the nervous system. Several instances of miR co-expression in the same direction as their target genes have been previously reported, albeit this is a less well understood phenomenon. We also detected a set of genes that, although presenting positive/negative co-expression, were not included in our list of in silico predicted targets, indicating that these genes are not potential miR targets according to our stringent criteria, however, they may be regulated by other mechanisms. In conclusion, comparing tumors of young patients with or without familial BC history not carriers of BRCA1/2 mutation our results showed similarity between their phenotypes, most tumors of the present series being of the luminal subtype corroborating previous results. However by applying co-expression analysis we found out transcriptional differences between both groups highlighting that changes in the miR-mRNA regulation were able to distinguish tumors between both groups. Cancer stem cells have been suggested to be responsible for the poor prognosis of patients with various cancers due to their characteristics and behavior, such as higher rates of therapeutic resistance and recurrence. Therefore, CSCs are regarded as a potential therapeutic target. To establish new treatments targeting CSCs, it is important to elucidate the molecular mechanisms underlying the acquisition of stemness in CSCs. However, these are still unclear, because CSCs are a rare population of cells in cancer tissue, and the rarity of the CSCs makes it difficult to identify and collect them.