HDAC7 (Histone Deacetylase 7)

SAHA imposes a common anti-proliferative core but engages distinct lineage-conditioned risk modules in LUAD and LUSC-cell-cycle/migration-linked in LUAD and checkpoint/stress-linked in LUSC. These SAHA feature-sensing modules provide a mechanistic and clinically anchored framework for subtype-tailored HDAC-directed combinations and for future development of HDACi-aligned biomarkers in NSCLC.

OLIG2 inhibition by either genetic deficiency or pharmacological targeting with CT-179 sensitizes GBM tumors to anti-PD-L1 therapy, enhancing antitumor immune responses and prolonging survival. Our findings reveal OLIG2+ glioma stem-like cells as critical mediators of immune evasion and identify the OLIG2/HDAC7/CXCL10 axis as a potential therapeutic target to enhance immune checkpoint inhibitors efficacy and to improve immunotherapy outcomes in aggressive GBM.

In LPS-treated cells, HDAC7 knockdown reduced TNF-α, IL-1β, IL-6 levels, and apoptosis, and increased cell viability, which also reversed by Nur77 knockdown. HDAC7 may inhibit Nur77 to exacerbate ARDS by upregulating Igkv14-126, IGLC2, Prss3b, and downregulating Ccdc50 and Chchd7, offering new targets for ARDS treatment.

We unveil MSN as a non-canonical GRK5/HDAC7 axis that promotes glioma malignancy by modulating the cortactin/MSN/CD44 pathway. Targeting this axis potentially represents a promising therapeutic strategy against gliomas.

This study evaluated daidzein's anti-leukaemic potential using integrated computational, in vitro, and in vivo approaches. Molecular docking and dynamics simulations confirmed stable HDAC7 binding with a binding affinity of -7.6 kcalmol⁻¹, comparable to vorinostat (SAHA; -6.7 kcalmol⁻¹)...HDAC7 suppression was further verified by immunohistochemistry in spleen and liver tissues. Moreover, peripheral blood mononuclear cell profiling showed enhancement of T cells and myeloid cells with concurrent reductions in B cells and macrophages, suggesting immunomodulatory potential.The demonstrated anti-leukaemic and immunomodulatory effects support further investigation toward potential clinical use.

Given the association of epigenetic regulation with chemotherapy resistance and cancer progression, this study aims to identify epigenetic vulnerabilities in two CRPC cell lines (DU145 and 22Rv1) established as resistant to two different taxanes, docetaxel (Dtx) and cabazitaxel (Cbz), using a small-molecule screening approach...Combination assays demonstrated that both compounds potentiated Dtx activity and helped overcome resistance in taxane-resistant CRPC models. This study highlights epigenetic vulnerabilities in taxane-resistant CRPC and identifies 4-Iodo-SAHA and SP2509 as promising monotherapy candidates, demonstrating their ability to potentiate Dtx activity and overcome resistance.

Additionally, a higher throughput thermal shift format was developed using dot blot analysis. Thermal shift analysis offers a useful complement to enzyme activity assays for characterization of HDAC inhibitors.

The identification of GCDH as a potential risk factor in HNC opens new avenues for targeted therapies, offering potential improvements in patient outcomes through precision medicine approaches.

HDAC7 represents a promising diagnostic and therapeutic target in BCa immunotherapy. Pinocembrin, as a specific HDAC7 inhibitor, holds potential as a combination therapy agent to improve immunotherapy response in BCa.

We then summarize the recent medicinal chemistry efforts, from the class-selective deacetylase inhibitors to the recently emerged targeted protein degraders that not only achieve superior isoform selectivity but also modulate HDAC7's deacetylase-independent functions. By bridging the functional complexity of HDAC7 with the latest advances in chemical biology tools, we aim to provide a timely summary of the current status of HDAC7 as a druggable target and offer a perspective on strategies guiding the development of next-generation modulators.

Furthermore, patient profiling based on the epigenetic state of the super-enhancers controlled by HDAC4 successfully identified a priori CRC patients resistant to platinum. This study supports HDAC4 as a key mediator of oxaliplatin resistance in FBXW7-mutated CRC and highlights the remodeling of a well-defined super-enhancer repertoire as part of the process of OXPT resensitization.

Chromatin immunoprecipitation (ChIP) assays confirmed that Harmine disrupts this interaction, liberating SP1 to bind the RECK promoter and activate its transcription. Collectively, these findings elucidate a novel HDAC7/RECK/SP1 axis through which harmine exerts its anti-metastatic effects in OC, highlighting its potential as a therapeutic agent for OC treatment.