CELF2 (CUGBP Elav-Like Family Member 2)

This study confirmed that RHPN1-AS1 expression inhibits the radiosensitivity of NPC cells. RHPN1-AS1 may affect NPC radiotherapy sensitivity by targeting CELF2 to regulate the MAPK pathway.

Functionally, Celf2 knockdown in ILPFC recapitulated the fear extinction memory deficit and reduced the number of dendritic spines. Together, these results indicate that lncRNA Dleu2 may serve as a potential therapeutic entry point for memory-related disorders.

In this exploratory analysis, we identified differentially methylated loci linked to thyroid cancer in Agent Orange exposed Veterans. Further research is necessary to replicate our findings in a larger cohort including Agent Orange exposure determination through biomarker assessment, and to elucidate mechanisms behind these associations in in vitro exposure models.

In summary, this study identified lncRNAs associated with NDMM and characterized LINC01432 as a critical regulator of MM cell survival, acting in complex with CELF2 to repress pro-apoptotic and immune response pathways. These findings highlight LINC01432 as a potential therapeutic target for overcoming resistance in MM.

CELF2 acts as a tumor suppressor in STAD by inhibiting proliferation, migration, and invasion, partly through regulating ADIPOQ and influencing the immune microenvironment. It represents a promising prognostic biomarker and new therapeutic target, with the CELF2/ADIPOQ axis offering a specific pathway for future drug development.

Moreover, Gene-TF and Gene-miRNA network analyses highlighted critical regulators, including TFs like CYR61, SMAD4, SOX2, TP63, and AR, along with miRNAs such as hsa-let-7b-5p, hsa-miR-34a-5p, hsa-let-7a-5p, hsa-let-7c-5p, and hsa-miR-16-5p, underscoring the functional impact of the selected features. In conclusion, the proposed approach effectively generates a streamlined set of optimal features, providing valuable biological insights and laying the groundwork for more accurate and effective tools in cancer diagnosis and prediction.

This study emphasized the impact of post-transcript regulation in the pathology of refractory JDM, highlighting the importance of regulating CELF2 PAS usage in the treatment of refractory JDM. Therefore, targeting proximal PAS usage may serve as a potential clinical biomarker and therapeutic strategy for managing refractory JDM.

The HNRNPC/CELF2 axis plays a pivotal role in metabolic reprogramming, driving AML progression and chemotherapy resistance. Targeting this pathway may offer new therapeutic strategies to overcome resistance and improve treatment outcomes in AML patients.

Fibroblast RBPs were dynamically regulated, particularly in extracellular matrix remodeling, with key proteins like CFL1 and PFN1 linked to improved prognosis. Furthermore, we identified heterogeneity in RBP regulation of the Macrophage Migration Inhibitory Factor (MIF) signaling pathway across cell types during the precancerous stage.ConclusionsOur findings highlight the crucial roles of RBPs in HNSC progression and suggest their potential as therapeutic targets and prognostic markers, offering insights into personalized treatment strategies.

CELF2 reduced the stability of CXCL5 and suppressed the proliferation and migration of bladder cancer cells by inhibiting p-AKT expression. The findings of this study highlight CELF2 as a potential therapeutic target for bladder cancer treatment.

This study profiles a comprehensive bcf-eccDNA landscape in patients with biliary strictures and offers valuable insights into eccDNA's role in bile liquid biopsy and carcinogenesis.

Based on this we propose that EZH2 exerts part of its oncogenic function in CML through the transcriptional repression of splicing factors. Finally, analysis of publicly available datasets suggests that splicing modulation by EZH2 might not be restricted to CML.