KDM5C (Lysine Demethylase 5C)

Notably, depleting ERRα markedly attenuates breast tumor cell growth in vitro and in vivo, and our in vitro evidence indicates this occurs in part through activating STING signaling. These findings establish that the ERRα-KDM5C serves as a critical checkpoint for STING enhancer activity, revealing a regulatory mechanism of STING enhancer activity in breast tumor progression.

These findings require prospective validation to confirm their clinical utility.

Blocking IL-6 synergistically augmented the antitumor efficacy of anti-PD-1 therapy. Our findings revealed a PBRM1-KDM5C-IL-6 axis that influenced antitumor immunity, indicating a potential immunotherapeutic strategy in PBRM1-deficient ccRCC.

Finally, integrative analyzes demonstrated strong correlations between promoter accessibility, transcription factor occupancy, and gene expression, and uncovered cooperation between epigenetic and genetic drivers. Together, these findings reveal context-dependent functional hierarchies among HMEs and underscore the necessity of multi-layered analyses to resolve the complexity of epigenetic regulation in cancer.

Consistently, in human brain tissue, JCV-infected glial cells displayed maintenance of a diploid chromosomal complement, likely through G2 arrest. The precise mechanism of this, however, remains to be elucidated.

The model (HNRNPM, HSPH1, JMJD6, KDM5C, LCK) effectively predicted prognosis and correlated with immune infiltration, tumor mutational burden, and drug sensitivity. This study provides insights into T-cell heterogeneity in LSCC and establishes a validated prognostic risk model for predicting survival and therapeutic outcomes.

Furthermore, we discuss emerging therapeutic strategies aimed at overcoming treatment resistance by targeting KDM5 demethylases. These insights provide a foundation for the development of innovative therapeutic interventions to enhance the efficacy of existing cancer treatments, offering a transformative approach to improving long-term patient survival and quality of life.

Future directions should integrate single-cell omics and targeted inhibitor development to elucidate microenvironmental interactions and enable precision therapies. This synthesis positions KDM5C as a pivotal epigenetic nexus in disease pathogenesis, offering context-dependent therapeutic opportunities.

TIA1 gene, stress granule (SG) marker, is tightly regulated by miR-33a/KDM5C/H3K4me3 axis and exosomal miR-33a diminishes the formation of stromal SGs in CAFs. Collectively, our study reveals tumour selectively secretes miR-33a-5p through EVs to remodel the stromal SG formation and gain survival possibility for cancer cells in tumour core region, highlighting a novel regulatory mechanism of iron and nutrient level on EV secretion and the function of polyamine metabolism in reshaping epigenetic profiles.

These findings highlight the potential of targeting KDM5C inhibition as a strategy for colon cancer treatment. Moreover, these findings underscore the promise of peptide inhibitors as targeted therapies, emphasizing their potential in altering the trajectory of cancer therapeutics.

Our prognostic model, factoring in T stage and genetic mutations in BAP1 and SETD2, effectively predicted recurrence in NMCCRCC patients. The potential of ctDNA as a non-invasive prognostic biomarker was underscored by its high detection rates and mutation concordance.

Significantly, the administration of the selective FUBP1 inhibitor, FUBP1-IN-1, is shown to effectively suppress CCDC183-AS1-induced PCa BM. These results shed light on the involvement of CCDC183-AS1 in enhancing osteoclastogenesis and the underlying mechanism in facilitating PCa BM, offering a potential avenue for therapeutic interventions.