MIR526B: MIR526B is a microRNA that has been studied in the context of breast cancer. Knockdown of MIR526B in highly aggressive COX-2/miRNA over-expressing cells has been shown to reduce oncogenic functions and reverse the epithelial-mesenchymal transition (EMT) phenotype [PMC5762661]. Bioinformatics analysis has revealed that both ZNF207 and NR2C2 are common targets of both MIR526B and miR655 [PMC7465874]. The mean expression data of MIR526B and miR655 has been presented as MIR526B cluster expression [PMC7465874]. Interestingly, miR655 appears to have a stronger role than MIR526B in the direct and indirect induction of oxidative stress [PMC6720387]. This suggests that hypoxia, MIR526B, and miR655 collaborate to enhance oxidative stress in breast cancer [PMC7465874]. The Pearson correlation coefficient (R) has been measured between each secretome marker and the expression of MIR526B or miR655 cluster in all breast cancer tumor subtypes [PMC10148110]. Furthermore, the expression of MIR526B and miR655 in human tumor tissue is significantly correlated with lymphangiogenesis markers VEGFC, VEGFD, and LYVE-1 [PMC6678879]. MIR526B is a microRNA that plays a role in breast cancer by influencing oncogenic functions and EMT phenotype. It shares common targets with miR655 such as ZNF207 and NR2C2. The expression levels of both microRNAs are correlated with lymphangiogenesis markers. Additionally, while both microRNAs contribute to oxidative stress induction, miR655 appears to have a stronger role than MIR526B. These findings suggest that hypoxia collaborates with both microRNAs to enhance oxidative stress in breast cancer. The expression levels of MIR526B and miR655 can be used to measure the correlation with secretome markers in breast cancer tumor subtypes.