MIR98 (MicroRNA 98)

The consistent alterations suggest the presence of a shared Notch-driven oncogenic signature in breast cancer, potentially driving cell proliferation, stemness, and resistance to therapy. These findings enhance our understanding of Notch signaling in breast cancer and propose novel miRNA-Notch interactions as candidate targets for therapeutic intervention.

These networks revealed several molecular modules associated with patient survival outcomes, such as the miR-200c-3p/ZEB2 axis in bladder cancer, the regulatory role of miR-98 in breast cancer, as well as the association of miR-21 with target genes APC in kidney renal cell carcinoma. These findings suggest that omics-specific clustering can identify robust survival-related patient clusters and uncover molecular features that may contribute to differential survival outcomes.

In vivo, miR-98-3p overexpression in subcutaneous xenografts resulted in reduced tumor volume, weight, vasculature, and blood perfusion, along with decreased expression of VEGFA, MMP2, and MMP9. These findings elucidate a MALAT1/miR-98-3p/VEGFA regulatory axis that modulates tumor angiogenesis in ovarian cancer, providing potential therapeutic targets for this malignancy.

However, 8-isoprostane levels were significantly lower in patients (6.68 pg/mL; interquartile range &lsqb;IQR]: 1.57-26.55) compared to controls (37.20 pg/mL, IQR: 18.55-167.58) (p < 0.001). Considering our findings in conjunction with existing literature, miR-98 appears to be a promising candidate biomarker for food allergy.

In addition, miR-98-5p can bind ELF3-AS1 and CPSF4 and down-regulate the expression of CPSF4. In summary, ELF3-AS1 promotes the proliferation, migration, and invasion of HCC cells by inhibiting miR-98-5p/CPSF4 axis.

&lsqb;This retracts the article DOI: 10.3727/096504016X14821952695683.].

Multivariable Cox regression analyses, adjusting for potential prognostic factors such as sex, Eastern Cooperative Oncology Group performance status, and tumor size and stage, revealed that CARS1-AS1 (adjusted hazard ratio &lsqb;HR] 0.33; 95% confidence interval &lsqb;CI], 0.15-0.73; P =0.0061) and miR-142-5p (adjusted HR 0.79; 95% CI, 0.61-1.01; P = 0.0581) were associated with improved overall survival. We identified potential Ex-smRNA biomarkers involved in PDAC progression and prognosis that reflect key molecular alterations in PDAC and may serve as clinically relevant biomarkers for disease monitoring.

The diagnostic model achieved an AUC of 0.956, a sensitivity of 94%, and a specificity of 93% in the training cohort and an AUC of 0.985, a sensitivity of 86%, and a specificity of 97% in the validation cohort. Our findings demonstrates that plasma sEV miRNA exhibits a highly discriminative biomarker for distinguishing NCs group from early malignant lesions, making it a promising tool for auxiliary detection of early-stage LC.

Moreover, along with the TCGA-validated hydroxyacyl-CoA dehydrogenase (HADH), the epithelial splicing regulatory protein-2 (ESRP2) and dihydrolipoamide branched chain transacylase E2 (DBT) were downregulated in both conditions, possibly attributed to the effect of functional hDEmiRs targeting them. Our findings offer potential candidates for miRNA-directed therapeutics in these pathologies.

This study underscores the potential of specific EV characteristics and microRNA content as early biomarkers for treatment response in patients with MS. The downregulation of specific microRNAs emerges as a promising indicator of favorable clinical outcomes, thereby suggesting their utility in early therapeutic decision making. Notably, our findings regarding miR-186-5p as a biomarker for brain atrophy represent a novel contribution to the field. Overall, early EV levels and microRNA content analysis at 3 months after treatment initiation seem to be promising as regards anticipating irreversible neurologic damage, thereby offering a valuable tool for optimizing MS treatment management.

Knockdown of IGF2BP3 enhanced erastin-induced ferroptosis sensitivity, marked by elevated MDA and ROS levels, reversible by ferrostatin-1...IGF2BP3 drives ferroptosis resistance in colon cancer by stabilizing SLC7A11 mRNA, while miR-98-5p antagonizes this pathway via IGF2BP3 downregulation. Targeting the miR-98-5p/IGF2BP3/SLC7A11 axis offers a promising therapeutic strategy to enhance ferroptosis sensitivity and improve colon cancer outcomes.

Besides, the suppression effects of miR-98-5p inhibitor on HUVECs proliferation, angiogenesis and metastasis was partly blunted by FOXN3 silencing. miR-98-5p released from CSWT-H9c2-OGD/R-Exo promoted HUVECs proliferation, angiogenesis and metastasis through directly targeting and suppressing FOXN3 expression.