DDX39B (DExD-Box Helicase 39B)

Thus, SNRPD2 maintains high DDX39B expression by preventing intron retention, and in turn, elevated DDX39B expression suppresses cryptic exon usage in CTSC to preserve CTSC expression, ultimately supporting malignant phenotypes of endometrial cancer. These results define a novel SNRPD2-DDX39B-CTSC regulatory axis and identify SNRPD2 as a promising therapeutic target for endometrial cancer.

Consistently, scRNA-seq analysis of human pancreatic patients showed increased MAP4K2 levels in infiltrating Treg cells. Collectively, MAP4K2 promotes Treg differentiation by inducing DDX39B nuclear translocation, leading to the attenuation of antitumor immunity.

We evaluated 5 recently established brain aging indices, which capture the heterogeneity of structural brain aging, in ADSP participants. R-indices replicated previously reported associations with AD groups (Yang et al., 2024), indicating the generalizability of the model. We identified different associations with genes that were previously linked to various traits. These findings provide new insights into the exploration of heterogeneity of neurodegeneration and related genetic risk factors.

Our identification of CPEB3, DDX39B, and SIDT2 as CRC revealed that CXCL12-related CRC biomarkers, combined with mechanistic evidence linking CXCL12 to MDSC regulation and anti-PD-L1 resistance, provides a novel framework for understanding immunotherapy failure in CRC. These findings might aid in establishing clinical CRC treatment strategies guiding the development of CXCL12-targeted combination strategies to overcome anti-PD-L1 resistance and improve CRC immunotherapy outcomes.

Functional validation demonstrated that DDX39B may represent a new therapeutic target for TNBC. Moreover, we identified a series of highly selective covalent probes targeting ARK1C1, PDIA1, and ALDH1A1, which could serve as valuable tools for detecting the expression and activity of these critical proteins.

RNA-sequencing variant calling and single-cell transcriptome projections revealed associations between these four TCs and germline variants. These findings support the potential of the identified WB-based transcriptional patterns to complement tumor characteristics in predictive and prognostic models for improved patient stratification.

According to structure-based virtual screening, we discovered a clinical antimalarial drug, artesunate, that disrupted the association of DDX39B-TRIM28 complex, resulting in DDX39B degradation and blocking the pro-metastatic effects of DDX39B. Overall, our findings uncover that TRIM28/DDX39B/ECAD axis contributes to NSCLC metastasis and targeting DDX39B degradation by artesunate is an effective and promising therapeutic approach for the treatment of NSCLC.

Notably, silencing of DCLK1-B effectively abrogated the pro-metastatic effects induced by DDX39B overexpression. Collectively, our results offered novel insights into the oncogenic role of DDX39B and highlighted its potential as a therapeutic target in COAD.

Patients in the low-risk group exhibited significantly improved outcomes (P = 0e + 00), underscoring the model's predictive accuracy. Notably, DDX39B and PRPF39 emerged as key splicing factors, exhibiting high expression in HNSCC and correlating with poor prognosis, positioning them as potential biomarkers and therapeutic targets.

This study demonstrates that SFPQ, DDX39B, and UBAP2 are significantly associated with poor prognosis in HCC, likely due to their roles in promoting angiogenesis and immune suppression. These findings highlight the potential of paraspeckle genes as prognostic biomarkers and therapeutic targets, offering new avenues for personalized treatment strategies in HCC. Further research into their functional mechanisms and clinical applicability is crucial for advancing HCC treatment and improving patient outcomes.

 Acin1 is overexpressed in HCC, and the overexpressed Acin1 is most likely regulated by miR-674-5p and other ceRNA molecules.

Taken together, these results identify relevant genes from both the MHC class I and II regions that are inflammation-responsive in cervical epithelium and associate with HPV (HCP5, HLA-B, HLA-C) and/or with genomic cervical cancer risk variants (HLA-DRB1, HLA-DRB6). They may thus constitute important contributors to the immune escape of precancerous cells after HPV-infection.