ESRP1 (Epithelial Splicing Regulatory Protein 1)

In conclusion, the lactylation-modified ESRP1/circPHGDH/miR-149/RAP1B axis drives the progression of PCa. These findings provide novel insights into the pathogenesis of PCa and suggest promising therapeutic targets for its treatment.

In contrast, Notch-related transcriptional readouts displayed distinct, context-dependent profiles across the examined identity states. Together, this study establishes a tractable non-transformed human model that captures selected molecular features associated with epithelial-mesenchymal plasticity beyond malignant contexts.

These findings suggest a novel role for ZEB1 in promoting ALT both transcriptionally and post-transcriptionally at multiple levels.

All cancer cells with stemness properties exhibit mesenchymal properties, but not all mesenchymal cells exhibit stemness properties. In summary, during EMT the stemness program is controlled by cell division and ESRP1, and this program predicts poor prognosis.

Prioritization of splicing events based on their likelihood to represent tumor antigens reveals that their aggregated load also correlates with high immune activity in multiple cancers, while also predicting expansion of T cells in BCs receiving ICB and prolonging long-term survival of cancer patients treated with ICB. Collectively, our method provides a framework for analyzing AS in single-cell data and defines a key role for AS in the response to ICB.

FGFR2-IIIc proportion represents a clinically relevant prognostic biomarker in advanced GC/GEJCs. Treatment-induced isoform switching toward FGFR2-IIIc suggests a novel resistance mechanism requiring targeted therapeutic approaches. These findings underscore the importance of developing isoform-specific therapeutic strategies and implementing FGFR2-IIIc assessment in precision oncology approaches for GC/GEJCs.

We also examine cancer-specific CD44 isoform expression patterns and assess their prognostic and therapeutic relevance. We propose that isoform-specific profiling of the CD44/ESRP1 axis may serve as a predictive framework for metastasis and therapy response, paving the way for targeted splicing-based therapeutics.

Our data indicate that PF from PM-PC patients is suitable for transcriptomic analysis. Numerous upregulated mRNAs known to play a role in tumour progression were identified. Our data indicate that mRNA profiling may be a clinically useful tool for further prognostic stratification of patients with proven PM, but larger studies are needed to validate our findings.

As a proof-of-concept, this study proposes tel46-functionalized CPG as a potential tool for isolating cancer-related proteins and underscores the potential of G4-interacting proteins as biomarkers for BC diagnosis and therapy. Moreover, these findings establish a basis for further research into G4-mediated cancer mechanisms.

Our results demonstrate that in RCC cells, ESRP1 promoter hypermethylation is accompanied by downregulation of its expression level; restoring ESRP1 expression can induce cell cycle G1-arrest and inhibit RCC cell proliferation by downregulating cyclin A2 expression; ESRP1-P-Luc2 may serve as a useful tool for monitoring the effects of DNMT inhibitor anticancer drugs at both the cellular level and in living animals, thereby providing a potential tool for high-throughput screening (HTS) of such drugs.

To investigate whether the presence of ER is a decisive factor in ESRP1's role, we treated ER-positive breast cancer cells with an ER inhibitor to induce EMT, followed by the knockdown of ESRP1, which further promoted the EMT process and enhanced the cells' invasive and migratory abilities. This study demonstrates that ESRP1 is a potential breast cancer prognostic marker with subtype specificity and its value as a molecular target needs to be accurately assessed in the context of breast cancer subtypes, as ESRP1 function may be highly dependent on the ER background.

Collectively, our findings reveal that ESRP1-derived circ_0008043 facilitates HCC cell migration and EMT by modulating the miR-661/PLEKHG4B axis, thereby promoting tumor metastasis. This study provides novel insights into the molecular mechanisms of HCC progression and suggests a potential therapeutic target for HCC treatment.