MIR508 (MicroRNA 508)

Bioinformatics analysis demonstrated high PLK2 expression was positively associated with oncogenes such as FAM163A, CTNND2, DAAM2, PITX1, POU1F1, mir-196a and negatively associated with tumor suppressors such as EMX2, PADI3, CDO1, SHOX2 and mir-508. In conclusion, the research elaborates on the expression profile and the clinical significance of PLK2 gene in AML, suggesting PLK2 expression may help risk stratification and hypothesis-generating for HSCT decision support.

These findings offer new insights into the occurrence and development of IDD and provide certain reference value for the subsequent diagnosis and treatment of IDD.

DEPDC1-AS1 may serve as a promising prognostic biomarker in EC. These findings suggest that DEPDC1-AS1 facilitates EC progression through the miR-508-3p, highlighting its potential as a therapeutic target.

AFAP1-AS1 accelerates the development of lung adenocarcinoma by cell proliferation, apoptosis, and invasion via the miR-508-3p/ZWINT axis. Thus, targeting AFAP1-AS1 or its downstream regulatory axis could offer novel therapeutic approaches in lung adenocarcinoma treatment.

miR-508-5p knockdown could inhibit the M2 polarization of TAMs by upregulating TSGA10, thereby suppressing the tumorigenic behavior of EC cells. miR-508-5p promotes the M2 polarization of TAMs and enhances the malignant behavior of EC cells by inhibiting TSGA10.

ARAP1-AS1 knockdown inhibited DLBCL tumor growth and reduced Ki-67, EMP1, and p-AKT expression in xenograft mouse models. ARAP1-AS1 knockdown exerts anti-tumor effect on DLBCL progression through the miR-508-5p/EMP1/PI3K/AKT axis.

The findings highlight the roles of DLL3 and miR-508-5p in EC. Targeting the miR-508-5p/DLL3 axis via exosome-mediated delivery represents a promising therapeutic strategy for EC.

eccMIR6748 also influences BC progression via the p38 mitogen-activated protein kinase (MAPK) signaling pathway. These findings suggest that eccDNAs, which contain functional genomic segments, play a role in BC initiation and progression, offering a dynamic source of genomic plasticity and potential as biomarkers and therapeutic targets.

A new prognostic model of MM associated with ARGs was created and validated, providing a new perspective for exploring the connection between ARGs and MM.

In addition, upregulation of DANCR is attributed to H3K27 acetylation at the promoter region. In conclusion, our study confirmed that activation of lncRNA DANCR by H3K27 acetylation has an oncogenic role in CRC progression and provides a potential therapeutic target for CRC.

Moreover, rescue experiment and tumorigenesis experiment in nude mice further confirmed that LncRNA PRKCA-AS1 regulates S100A16 through sponging miR-508-5p to regulate LUAD progression in vitro and in vivo. These results demonstrated that LncRNA PRKCA-AS1 might regulate LUAD by acting as a ceRNA via sponging miR-508-5p and regulating S100A16 expression, indicating that manipulation of PRKCA-AS1 might be a potential therapeutic strategy in LUAD.

In vivo, nude mouse xenograft experiments demonstrated that circDNAH14 knockdown augmented the hypoxia-induced suppression of HCC tumor growth. In conclusion, circDNAH14 mitigates the suppressive effects of hypoxia on HCC, both in vitro and in vivo, by competitively binding to miR-508-3p and regulating PTMA expression.