LINC00958 (Long Intergenic Non-Protein Coding RNA 958)

Collectively, our findings demonstrate that GR inhibits CC through a ncRNA-mediated suppression of CDK2, leading to reduced HeLa cell proliferation and migration and enhanced apoptosis. These results provide a mechanistic rationale for developing GR as a candidate agent for targeted therapy and immuno-combination strategies in CC.

Overall, this study identifies LINC00958 as a novel oncogenic lncRNA in EC, which facilitates tumor progression by sponging miR-129-2-3p and enhancing NOTCH3 signaling. These findings provide new insights into the molecular mechanisms of EC and suggest that targeting the LINC00958/miR-129-2-3p/NOTCH3 axis may represent a promising therapeutic strategy.

Verification of methylation levels indicated that KIAA1429 overexpression resulted in heightened methylation of LINC00958. It was concluded that KIAA1429 diminishes the proliferation, invasion, and tumorigenesis of cancer cells through the methylation of LINC00958.DiscussionThis research provided insights into the role of LINC00958 in oral cancer cells and underscored the impact of methylation, offering a theoretical foundation for improving clinical diagnosis and treatment strategies for oral cancer patients.

Furthermore, LINC00958 combined with glioma-associated oncogene homolog 1 (GLI1) to activate Hedgehog pathway, thereby promoting M2 polarization. Exosomal LINC00958 maintained OC cell stemness and induced M2 polarization via the Hedgehog signaling pathway.

AFAP1-AS1 is an oncogene that aggravates the development of OSCC via the ubiquitin-mediated proteolysis pathway. It also provides a novel potential therapy for OSCC.

Finally, we show that LINC00958 can be used as a predictor of relapses in patients who are usually stratified as standard risk and thus not always targeted for marrow transplantation. Our results open the way to new diagnostic perspectives that can be directly used in clinical practice for a better management of B-ALL paediatric patients.

miR-27b-5p was significantly associated with LINC00958, and downstream NT5E predicted poor survival in HNSCC cases. LINC00958 may affect the prognosis by regulating NT5E via miR-27b-5p, and could serve as a possible factor to predict the prognosis of HNSCC, especially oral squamous cell carcinoma.

Overall, The results of this study show that LINC00958 and miR-627-5p may be used as new diagnostic markers for LSCC. In addition, LINC00958/miR-627-5p axis opens a new way for the diagnosis and treatment of LSCC.

LINC00958 interacts with miR-145-3p and modulates the miR-145-3p/CDK1 axis. Hence, LINC00958 contributes to CC's malignant progression.

In BC, LINC00958 is highly expressed while miR-625-5p is underexpressed. LINC00958 can inhibit cell autophagy to enhance cell activity; promote OS, inflammation, and AG; and regulate tumor immunity by targeting miR-625-5p, thus participating in the development of BC.