hsa-mir-622: Hsa-mir-622 is an intriguing microRNA that is coded within the keratin 18 pseudogene 27 (KRT18P27) [PMC9851309]. It is one of several microRNAs that have been found to promote tumor growth, including hsa-mir-622, hsa-miR-650, hsa-miR-223, hsa-miR-21, and hsa-miR-181a [Zhang et al., 2010, 2012a,b; Guo et al., 2011; Li et al., 2011b]. On the other hand, there are microRNAs such as hsa-miR-107, -145, -495, -551a, let-7f, -218 and -610 that have been shown to inhibit cell invasion and metastasis [Tie et al., 2010; Li et al., 2011a,b; Liang et al., 2011; Feng et al., 2012; Gao et al., 2012; Wang et al., 2012] [PMC3521996]. Somatic mutations have been identified in several miRNA genes including hsa-mir-622 [PMC3334977]. Furthermore, it has been found that hsa-mir-622 is downregulated in certain conditions and has predicted target genes such as G3BP1 and CELF2 [PMC4966693]. Additionally, there is evidence to suggest that circRNA_050263 and circRNA_003022 can target hsa-mir-622 among other microRNAs [PMC9658433]. Existing evidence confirms the presence of seven variants of hsa-mir-622 [PMC9389118]. Finally, a study identified eleven miRNAs in common with existing evidence including hsa-mir-622 [PMC9252828]. Overall, hsa-mir-622 has been found to play a role in tumor growth, cell invasion, and metastasis, and has been associated with specific target genes and somatic mutations.

MIR622: MIR622 is a microRNA that is both induced and suppressed upon differentiation [PMC4168020]. It has been found to play a role in desensitizing PARP inhibitors by downregulating the expression of Ku 70/80, which reduces non-homologous end joining (NHEJ) activity and restores homologous recombination (HR) activity [PMC9455597]. In various studies, MIR622 has been identified as one of the differentially expressed microRNAs in different conditions. It was found to be differentially expressed in most repetitions performed, along with MIR34A*, MIR126*, and MIR30D [PMC3123620]. Additionally, it has been analyzed for expression analysis in patients with different Ross scores [PMC5578659]. In hepatocellular carcinoma (HCC), increased expression of MIR622 has been associated with sorafenib resistance and activation of various pathways such as the RAS-ERK pathway and PI3K-AKT pathway [PMC8007794]. However, miR122 and miR137 have shown inhibitory effects on sorafenib-resistant cells through the AKT/ERK pathway [PMC8007794]. Overall, MIR622 appears to have diverse roles in cellular processes such as differentiation, PARP inhibitor sensitivity, and resistance to therapy.