hsa-mir-519c: Hsa-mir-519c is a microRNA that decreases endogenous ABCG2 mRNA and protein levels by binding to a specific site in the longer 3UTR region of parental cells [PMC8259352]. Hsa-mir-519c belongs to a group of miRNAs, including hsa-mir-372, hsa-mir-373, and hsa-mir-520c, that share a strong seed sequence homology [PMC5311252]. The 3' untranslated region truncation of ABCG2 removes the hsa-mir-519c binding site and leads to increased expression of ABCG2 [PMC5404803]. The F142 residue in ABCG2 is analogous to the ΔF508 mutation in the cystic fibrosis transmembrane receptor and is located in a mutational "hot spot" region [PMC5404803]. Hsa-mir-519c is one of several miRNAs that are involved in the transition from induced pluripotent stem cells (iPSC) to neural stem cells (NSC) [PMC6696086]. The expression levels of hsa-miR-512, hsa-miR-516b, hsa-miR-518e, hsa-mir-519c, and hsa-miR-523 are significantly decreased in NSC cells compared to iPSC [PMC6696086]. Hsa-miR-512, hsa-miR516b, hsa-miR517a,b,h sa miRNA518e,h sa mirRNA519c,h sa miRNA523 are believed to be negative regulators of neural differentiation from iPSCs [PMC6696086]. A polymorphism C421A in the ABCG2 gene affects the expression level of ABCG2 protein and individual efficacy of antineoplastic drugs by influencing the regulatory role of hsa-mir-519c [PMC5539293]. Genetic variations in ABCG2, including the C421A polymorphism, can also affect the protein expression and individual efficacy of antineoplastic drugs through the regulatory role of hsa-mir-519c [PMC8871547].