HNRNPK (Heterogeneous Nuclear Ribonucleoprotein K)

This trimer stabilizes STAT3-enhancer-promoter loops (EPLs), thereby reinforcing the Tns1 transcription and facilitating CRCLM. Our findings elucidate the mechanism by which E. coli-induced NETs promote CRCLM through epigenetic modifications, offering an insight into the role of EPLs in immune regulation and tumor progression.

Among these hub proteins, five proteins (NPM1, TOP2A, EZH2, PRKDC, and HNRNPK) were identified as clinically relevant when cross-referenced with the Human Protein Atlas database and the literature, highlighting their potential as diagnostic and therapeutic targets. These findings highlight the potential of nanoMIP-based snapshot imprinting as an alternative to 'classical' approaches for identifying potential protein targets for diagnostic and therapeutic applications.

Rescue experiments demonstrated that TL1A knockdown in hnRNPK-overexpressing cells significantly reversed pro-tumor phenotypes, suggesting that hnRNPK exerts its oncogenic effects at least partially through a TL1A-dependent mechanism. These findings not only provide insights into the molecular mechanism of hnRNPK in GC but also offer experimental evidence for developing novel therapeutic strategies targeting the hnRNPK-TL1A axis in GC.

These findings demonstrate the utility of NMF for characterizing the contribution of genes to repair pathways and provide a foundation to discover new gene functions in DSB repair. github.com/joanagoncalveslab/MuSpectraNMF .

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.

Our findings uncover a novel mechanism by which DDX1 crotonylation regulates the AS of peroxisome-related genes and mediates peroxisomal redox homeostasis. This discovery bridges a critical gap in our understanding of how posttranslational modifications (PTMs) of DEAD/DEXD box RNA helicases modulate gene AS and identifies a potential therapeutic target for colorectal cancer.

The serum level of circSMEK1 has non-invasive diagnostic value for HCC (AUC = 0.790), as well as potential diagnostic utility for early HCC or high-risk MASH, owing to its key role in bridging MASH to HCC progression. Restoring of circSMEK1, alone or combined with IGF2 inhibitors, proposing a novel therapeutic strategy for HCC.

Metastatic tumor cells display profound immunometabolic plasticity to colonize distant organs. We identify IMPACT, an inhibitor of GCN1-stress signaling, expression of which curtailed metabolic plasticity and augmented tumor immunogenicity, sensitizing metastatic tumor cells to NK cell-mediated destruction.

These findings reveal a novel mechanism by which circPVT1 contributes to RCC, highlighting the potential of the cP104aa peptide as a therapeutic target. Axitinib may serve as an effective therapeutic agent for patients with advanced RCC exhibiting high cP104aa expression.

Analysis across cancer cell lines revealed that sensitivity to CMP76 was significantly associated with RBM42 dependency. This work establishes a novel therapeutic strategy to inhibit MYC translation mediated by hnRNPK, offering a translationally targeted approach to cancer therapy.

Strikingly, combining Remodelin with the YAP1 inhibitor Verteporfin synergistically augmented anti-PD-1 efficacy, significantly suppressing tumor growth in immunocompetent mouse models. Our findings not only elucidate an ac4C-dependent epitranscriptomic mechanism governing vascular-immune crosstalk but also propose a novel combinatorial therapeutic strategy to overcome resistance to immune checkpoint blockade in GC.