H2BC8 (H2B Clustered Histone 8)

LDOC1-mediated chromatin remodeling, through regulation of H2Bub1 recruitment and turnover, represents a key mechanism promoting NSCLC progression. The LDOC1-H2Bub1 axis, potentially involving THAP12, shapes chromatin accessibility and metastatic transcriptional programs, providing mechanistic and clinical insights into tumor aggressiveness and therapeutic response.

Gene-disease interaction analysis revealed Metastasis-associated lung adenocarcinoma transcript-1 (MALAT1) and histone cluster 1, H2bc (HIST1H2BC) as the most relevant diagnostic biomarkers. Thus, the dg IDB database provided potential for drug repurposing, targeted therapy and broad-spectrum antiviral applications.

The CAFLUX HepG2 reporter system therefore provides a sensitive and reproducible platform for real-time, nuclear-localized monitoring of AhR-mediated gene expression. Its responsiveness to both agonists and antagonists underscores its potential utility in toxicological evaluation, drug discovery, and the investigation of EV-mediated signaling in liver cancer models.

In preclinical models, systemic p300/CBP degradation inhibited tumor growth, synergized with AR antagonists and showed no evident toxicity. These findings position H2BNTac as an epigenetic marker of enhancer addiction and establish dual p300/CBP degradation as a promising therapeutic strategy for enhancer-driven cancers.

RNF20-silenced A549 cells exhibited heightened sensitivity to both the Cisplatin and PARP inhibitor Olaparib. These findings provide an important foundation for further understanding the molecular mechanisms of lung adenocarcinoma and developing new treatment strategies.

Mechanistically, Rnf20 knockdown in adipocytes reduced H3K4me3 occupancy at the Slc2a4 gene locus, inhibiting GLUT4 expression and inducing adipose-specific insulin resistance. These findings establish a critical role for adipocyte RNF20 in the insulin signalling regulation via the H2Bub-H3K4me3-Slc2a4 axis, highlighting its importance in systemic glucose metabolism.

Among these, filamin C (FLNC), leucine zipper protein 1 (LUZP1), and glutamate-rich WD repeat-containing protein 1 (GRWD1) showed higher expression on stiff substrates, with GRWD1 known for its role in cancer progression through cell cycle and gene regulation. These findings highlight how substrate stiffness modulates gene expression via UBE2A/B-mediated H2B ubiquitination.

Our findings reveal that lactate-driven epigenetic modification via the LDHA-NDRG1 axis creates a molecularly distinct subpopulation enabling senescence resistance, providing mechanistic insights into HCC heterogeneity. This work proposes a precision medicine strategy targeting lactylation-mediated epigenetic regulation, with implications for developing combination therapies and patient stratification based on clonal evolution patterns.

We demonstrated that H2BC9 expression may be associated with HNSCC development and prognosis. These findings may provide a potential therapeutic target for HNSCC.

Different tumor models in vivo demonstrated that DTX2 inhibitor treatment inhibited tumor growth and sensitized HCC cells to the therapeutic effects of programmed cell death protein 1 (PD-1) antibody. In summary, this study identifies DTX2 as a potential target for HCC immunotherapy.

According to our study, the reactome pre-Notch expression including POGLUT1 and HIST1H2BC was associated with a risk of Hepatitis B in Taiwanese men when compared to women.

Cluster analysis shows that low ESRP1 expression correlates with enhanced immune activity, predicting better prognosis. This discovery suggests that ESRP1 can serve as a potential biomarker for the prognosis of PAAD, offering new insights into personalized immunotherapy by influencing immune regulation and tumor progression.