ELAVL1 (ELAV Like RNA Binding Protein 1)

This study establishes a regulatory network linking arecoline/4-NQO, AKT1, m6A factors, and OSCC, and identifies key molecular targets and mechanisms underlying the carcinogenic process. These findings provide a theoretical foundation for understanding the pathogenesis of OSCC and developing targeted strategies for early intervention and treatment.

In summary, ELAVL1 promotes LNM in PTC by stabilising PDE4C. Our study elucidates the molecular mechanisms driving PTC metastasis, offering new therapeutic avenues for PTC treatment.

Conversely, ELAVL1 knockdown significantly inhibited proliferation, induced G1 phase arrest, decreased S phase cells, and significantly decreased COX-2 and PGE2 expression. These findings indicate that ELAVL1 promotes proliferation and inhibits apoptosis in MDV-transformed MSB1 cells, potentially via the COX-2/PGE2 signaling pathway.

SNHG12 knockdown inhibits DTX resistance of PCa cells by reducing SNHG12 binding to ELAVL1 to inhibit the activation the PI3K/AKT signaling pathway.

Additionally, we found that a colon cancer-associated SNP in the POU2AF2/C11orf53 3'UTR creates an ectopic DplUSE site, increasing gene expression in zebrafish gut cells and in a human cell line. We have therefore identified a short 3'UTR motif present in diverse vertebrate genes that controls their expression through conserved RBPs interactions and is implicated in human disease.

When heterogeneous nuclear ribonucleoprotein K (hnRNPK), an ITAF for the HTLV-1 IRES but not for the sHBZ IRES, is overexpressed with HuR, HTLV-1 IRES is stimulated, whereas sHBZ IRES activity is reduced. Consequently, ITAFs or combinations of ITAFs differentially modulated the HTLV-1 IRES and sHBZ IRES activity, indicating that these IRESs are under translational control mediated by different subsets of ITAFs.

In macrophages, overexpressed ELAVL1 promoted autophagy, and the autophagy activator Rapamycin reversed LINC01943-induced M2 polarization. Overall, this study found that RT upregulates hnRNPA2B1 to stabilize LINC01943 expression and enhance its Exo-mediated release, which subsequently inhibits ELAVL1-dependent autophagy in macrophages, accelerating M2 polarization.

Furthermore, correlation with clinical data from the TCGA database revealed that m6A-associated DEGs, such as HMGA1, ERO1A, LRFN4, SNTN, SLC2A1, DNASE2B, and VSIG2, were prognostically significant in NSCLC. This study underscores the pivotal role of m6A modifications in NSCLC and highlights the potential of dRNA-seq for identifying RNA epigenetic changes that may serve as novel therapeutic targets.

Notably, HuR-driven TME remodeling reinforces environmental stressors that further activate HuR, establishing a feed-forward loop that drives disease progression. These findings underscore HuR as a central regulator of the PDAC TME and therapeutic resistance, and thus, highlight its potential as a target in PDAC.

Given the role of BMP2 in modulating the tumor microenvironment and its association with bone-invasive phenotypes, it holds potential as a predictive biomarker for response to ultrasound-enhanced therapeutic strategies. ELAVL1-regulated BMP2 promotes OSCC progression and bone infiltration and may serve as a valuable predictive biomarker for therapeutic response in ultrasound-guided biotherapies.

Furthermore, elevated serum exosomal circ_0008803 levels correlated with advanced NSCLC stages and distant metastasis. In summary, this study highlights circ_0008803 as a novel exosomal circRNA implicated in NSCLC metastasis, providing mechanistic insights and underscoring its potential as a diagnostic biomarker.

ELAVL1 is highly expressed in HSPC. High expression of ELAVL1 is associated with the proliferation of HSPC. SOX4 is a downstream molecule of ELAVL1 which promotes the proliferation of HSPC. ELAVL1 enhances the stability of SOX4 mRNA through an m6A-dependent mechanism.