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MIR193A is a microRNA that has been studied in various diseases, including primary focal segmental glomerulosclerosis (FSGS), minimal change disease, and hepatocellular carcinoma (HCC) [PMC9953542] [PMC7226544] [PMC9562882]. In primary FSGS, MIR193A is found to be overexpressed in podocytes, while genetic FSGS and minimal change disease exhibit low levels of MIR193A similar to normal kidneys [PMC9953542]. This suggests a potential causal relationship between the expression of the vitamin D receptor/retinoid X receptor (VDR/RXR) and the downregulation of MIR193A in these diseases [PMC7226544]. In breast cancer cells, overexpression of MIR193A inhibits micro-vessel formation by 40% compared to control cells [PMC9562882]. The expression levels of MIR193A by precursor progenitor cells determine their net phenotype as either podocytes or parietal epithelial cells through modulation of WT1 gene expression [PMC9953542]. The position of the 3' untranslated region (UTR) plays a significant role in miRNA activity, with an ideal distance from the stop codon or seed location for optimal MIR193A activity [PMC7226544]. In HCC, downregulation of miR-23b and MIR193A may contribute to disease diagnosis and miR-193a could be a prognostic factor for HCC patients. DNA methylation mediates miR-23b expression but not miR-193a in primary HCC [PMC5351682]. Transcription factors such as YY1, WT1, and Sox2 may regulate MIR193A expression by binding to its promoter region. Additionally, exosomes secreted by advanced mouse colon cancer cells contain MIR193A, a tumor suppressor miRNA, along with MVP [PMC7916137]. MIR193A has also been suggested to bind to the mRNA of the APOL1 3' UTR region, and the expression of APOL1 in podocytes is associated with the regulation of MIR193A and actin cytoskeleton organization [PMC7226544] [PMC8391400].