KDM5B (Lysine Demethylase 5B)

KDM5B upregulation was significantly negatively correlated with the survival rates in various cancer types, including thyroid, lung, esophageal and colorectal cancers. Overall, these findings establish a novel regulatory axis in cholesterol metabolism, uncover potential therapeutic vulnerabilities in ER+ breast cancer, and suggest that targeting the KDM5B could provide a strategy to curb tumor progression.

Through this comprehensive characterization, KDM5B-depleted microglia exhibited broad remodeling of immune reactivity, including reduced intracellular and secreted inflammatory responses to lipopolysaccharide as well as distinct modulation of alcohol- and interleukin-4-induced pathways, that was functionally demonstrated by altered cytokine secretion profiles. Results from this study provide critical insight into KDM5B-mediated immunological effects on microglial function.

Fifty male C57BL/6 mice were randomized into control, model, XLP(2.7, 5.4 mg·g~(-1)), and 5-aminosalicylic acid+fluoxetine groups...Furthermore, XLP lowered the levels of TNF-α, IL-1β, IL-6, and IL-23, down-regulated the transcript levels of IL-6 and IL-23α and the protein level of H3K4me3 while up-regulating the protein level of KDM5B in the cerebral cortical area and the colon tissue, and increased the binding of KDM5B to the IL-6 and IL-23α promoters. XLP may affect H3K4me3 demethylation through KDM5B to reduce the production of inflammatory factors and alleviate the inflammatory response, thus ameliorating UC combined with depression.

An inactivating ASXL1 variant and an in-frame KDM5B::LPGAT1 fusion were identified in one melanoma; paternal disomy of 11p15.5 in both embryonal rhabdomyosarcomas. Mesenchymal tumors and melanomas showed distinct transcriptional profiles enriched in muscle and synapse organization and epidermal differentiation genes, respectively.

Additionally, in in vivo organoid models, cisplatin (CDDP) induced ferroptosis combined with GABPA inhibition demonstrated superior anticancer effects compared to conventional platinum-based drugs. This research identifies new targets and regulatory networks that hold promise for developing ferroptosis-based therapies for KRAS-mutant LUAD.

Knockdown of JARID1B in human G3MB cell lines reduced growth, supporting potential as a therapeutic target. We conclude that a MYC-TGFβ-JARID1B axis represses target genes to drive G3MB and present new humanized models for G3MB to understand epigenetic dysregulation in G3MB.

Drug sensitivity profiling highlighted differential therapeutic vulnerabilities between risk groups. This study established and validated a novel CTA-based prognostic tool for prognostic stratification and personalized treatment guidance in AML, bridging molecular insights with clinical applications.

Importantly, combining GTN with the ferroptosis inducer RSL3 synergistically enhances antitumor efficacy in vivo. Our study unveils a previously unrecognized KDM5B/ferroptosis axis through which GTN exerts its antitumor effects, positioning GTN as a promising lead compound for ferroptosis-targeted therapy in RCC.

Collectively, these results indicated that Casticin suppresses and sensitizes non-small-cell lung cancer cells to EGFR-TKIs. Casticin may serve as a sensitizing agent by targeting SMYD2 to improve the efficacy of EGFR-TKIs.

This comprehensive transcriptomic characterization of T-cell exclusion in PM reveals that targeting cilium-based Hedgehog signaling, in addition to multiple other actionable drug targets, could enhance the efficacy of ICB treatment in PM.

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.

We identified six biomarkers, namely ARF6, ASF1B, CHD5, FLNA, KDM5B, and SPI1, thereby establishing a theoretical foundation for clinical diagnosis of AML.