MIR22HG (MIR22 Host Gene)

This series offers an integrated clinicopathological and molecular overview of diagnostically challenging nodular fasciitis, emphasising the importance of including it in the differential diagnosis of mesenchymal tumours in both superficial and deep sites. We believe this series contributes to the understanding of USP6-associated neoplasia and will aid pathologists in recognising nodular fasciitis in challenging settings, enhance diagnostic confidence, and support targeted use of advanced molecular techniques.

Collectively, our data delineate an SIN3A-MIR22HG-Beclin1 regulatory axis that links RNA-level repression to autophagy and ferroptosis control in LUAD and suggest that disruption of this pathway contributes to tumor progression. Targeting SIN3A-mediated repression of MIR22HG may, therefore, represent a potential therapeutic avenue for LUAD.

Therefore, MIR22HG may function as a competing endogenous RNA (ceRNA) to regulate miR-4428/PCDH9. We demonstrated that MIR22HG acts as a tumour suppressor in Pca and suggested that targeting the MIR22HG/miR-4428/PCDH9 axis may be a new avenue for Pca therapy.

MIR22HG serves as a tumor suppressor in ATC and impedes the progression of ATC through regulation of miR-141-3p/PTEN/AKT axis. Our findings illustrate the critical role of the MIR22HG/miR-141-3p/PTEN/AKT axis in the progression of ATC, which offers new insights for the therapeutic strategies of ATC.

Additionally, loss-and-gain-of-function assays demonstrated that overexpression of MIR22HG led to the upregulation of NFAT5, which mitigated renal apoptosis, and inflammation and improved renal function. Collectively, the results of our study highlight the therapeutic potential of targeting the MIR22HG/miR-134-5p/NFAT5 axis in the treatment of ischemic AKI, providing new insights into the molecular regulation of renal cell survival and repair during injury.

In recent years, it has been shown that dysregulation of molecular mechanisms in many LncRNAs such as MIR22HG, HULC, AGAP2-AS1, MALAT1, PVT1, TTTY14, HOTAIRM1, PTAR, LPP-AS2, LINC00336, and TINCR are connected with the GBM. Therefore, this scientific review paper focused on the molecular mechanisms of these LncRNAs in the context of GBM.

We found that miR-22-3p intracellular effects result at least partially from the targeting of the mRNA encoding the deacetylase sirtuin-1 (SIRT1), a well-established pro-survival factor. Therefore, this novel XBP1s/miR-22/SIRT1 axis identified could play a pivotal role in the proliferation and chemotherapeutic response of leukemic cells.

Our study revealed the requirement for site-specific methylation of lncRNAs in the tumorigenesis of GCSCs, contributing novel insights into cancer development.

Furthermore, the study predicted that CRNDE may exhibit oncogenic features by adsorbing miR-23b-3p and positively regulating IDH1 expression. Overall, the study constructed a prognostic model in glioma, and predicted a lncRNA CRNDE/miR-23b-3p/IDH1 axis, which could potentially be useful for gene therapy of glioma.

Additionally, transwell assays showed that knockdown of LINC00923 and LINC01341 significantly attenuated the invasive and migratory capacities of H226 and H1703 cells. This study has identified 12 candidate lncRNA associated with prognostic implications, among which LINC00923 and LINC01341 exhibit potential as markers for the prediction of LUSC outcomes.

Thus, the regulation of MIR22HG-HuR/BCL-2 and MIR22HG/HMGB1 signaling pathways is involved in the anti-HCC proliferation and metastasis effects of Andro. This study provided a new pharmacological basis for Andro in HCC treatment and, for the first time, identified a natural product molecule capable of positively regulating MIR22HG, which has a robust biological function.

In conclusion, MIR22HG in SCLC was found to modulate miR-9-3p level and might act as a possible biomarker for SCLC treatment.