MIR221: MIR221 is a microRNA that has been studied in various contexts [PMC7318537]. Annexin V analysis showed significantly more apoptotic cells among cells transfected with the MIR221 inhibitor than among those transfected with the MIR221 mimics [PMC7318537]. In LX2 cells, the overexpression of MIR221 mimics resulted in the aggregation of P62, indicating autolysosome dysfunction [PMC8436230]. The effects of GATA4-Exo, the MIR221 inhibitor, and PTEN deletion on p-Akt and c-Cas-3 expression were tested after hypoxia stimulation [PMC7318537]. In a study analyzing microRNAs in hyperlipidemia-related diseases, including atherosclerosis, non-alcoholic fatty liver disease (NAFLD), obesity, and type II diabetes (T2DM), it was found that both miR155 and MIR221 were significantly modulated in all four diseases [PMC7604447]. Several miRNAs, including MIR21, MIR221, MIR222, MIR26, and MIR19 have been shown to function as oncomiRs by targeting PTEN expression and promoting cancer cell growth [PMC4389881]. The expression level of MIR221 was normalized to U6 RNA [PMC8327461]. Additionally, aberrant expression of miRNAs such as miR34, miR36, miR21, miR203 was observed in breast cancer along with upregulation of both MIR221 and MIR222. This upregulation correlated with downregulated p53 gene profile and activation of oncogenic pathways such as PI3K-Akt-mTOR signaling [PMC8071157].