hsa-mir-612: Hsa-mir-612 is one of the seventeen miRNAs selected as potential regulators of the VEGFA gene [PMC7444729]. In a study, wild-type and mutant fragments of the 3'-untranslated region (UTR) in circETFA or CCL5, which may bind to hsa-mir-612, were designed and inserted into a reporter vector [PMC8556257]. These reporter genes were then co-transfected into 293 T cells along with hsa-mir-612 mimic or inhibitor [PMC8556257]. The purpose of this experiment was to investigate the potential regulatory role of hsa-mir-612 in the expression of circETFA and CCL5 [PMC8556257]. The study aimed to determine whether hsa-mir-612 could bind to the 3'-UTR fragments and affect gene expression [PMC8556257]. The results would provide insights into the regulatory mechanisms involving hsa-mir-612 and its potential role in modulating VEGFA gene expression through its interaction with circETFA or CCL5 [PMC7444729][PMC8556257]. Further research is needed to fully understand the functional significance of this interaction and its implications in disease processes.

MIR612: MIR612 is a miRNA that has been studied in various contexts. In a study comparing multiple sclerosis (MS) and vitiligo, MIR612 was found to be one of the genes that showed similar expression in both conditions [PMC7953917]. Additionally, MIR612 was identified as one of the miRNAs that were highly expressed in glioblastoma stem cell lines and were also found to be common in the Glioblastoma Bio Discovery Portal of the TCGA database [PMC8911495]. Another study identified MIR612 as one of the miRNA genes with a peak center located in its promoter region [PMC9519027]. In a different study, downregulation of MIR612 was observed along with other genes such as UBE2W, HECTD1, ATRX, SOX4, HBP1, and Fgl2 [PMC6300492]. However, this downregulation was not confirmed by qPCR for UBE2W, HECTD1, ATRX, and SOX4 [PMC6300492]. Furthermore, MIR612 has been investigated for its role in inhibiting epithelial to mesothelial transformation (EMT) by suppressing invadopodia formation and rearranging MMPs and other adhesion molecules [PMC7006096]. Lastly, it has been reported that H19 enhances cholangiocarcinoma development by inhibiting MIR612 expression and promoting Bcl-2 expression [PMC10037657]. Overall, these studies highlight the involvement of MIR612 in various biological processes and diseases.