ArticleCell biochemistry and biophysics2026
Histone Deacetylase Inhibitor Panobinostat Augments the Antitumor Efficacy of Bromodomain Inhibitor JQ1 by Hijacking Mechanisms of Apoptosis in Head Neck Squamous Cell Carcinoma.
Article in Cell biochemistry and biophysics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
BRD4 is frequently overexpressed and associated with poor prognosis, making it a promising therapeutic target in head and neck squamous cell carcinoma (HNSCC). BRD4 inhibitors such as JQ1 have demonstrated anti-tumor activity in preclinical HNSCC models, but their efficacy is often limited by adaptive resistance and dose-related toxicity. Combination strategies may help overcome these limitations by enhancing therapeutic efficacy and reducing the dose-limiting toxicities associated with monotherapy. This study aimed to identify novel agents that can be synergized with JQ1 to enhance its therapeutic effect and overcome resistance in HNSCC. A drug synergy screen that combined JQ1 with 7 well characterized epigenetic drugs was used for potent anti-cancer properties in HNSCC, and initially found histone deacetylase inhibitor (HDACi) Panobinostat (PAN) had synergistically anti-tumor effects with JQ1 in HNSCC cell lines. Cell proliferation and apoptosis were examined by CCK-8 viability assay, colony formation assay and flow cytometry analysis. 4NQO-induced animal model and subcutaneous xenograft animal model were used as the primary model systems. RNA sequencing (RNA-seq) was conducted to identify differentially expressed genes (DEGs) modulated by JQ1 and PAN in HNSCC cells, followed by functional analysis using bioinformatics. Integrative rescue experiments and luciferase assays were performed to characterize the key mediators underlying the therapeutic effects of JQ1 and PAN. Co-treatment of JQ1 and PAN synergistically suppressed cell proliferation and induced cell apoptosis in vitro. Preclinical animal studies showed that dual inhibition of BRD4 and HDAC significantly inhibited tumor progression and growth in vivo. Differentially expressed genes (DEGs) modulated by JQ1 and PAN were significantly enriched in apoptosis, cell cycle, p53 pathway and pathway in cancer. DEG-associated prognostic risk score robustly stratified HNSCC patients into subgroups with high or low survival. BGN was considered as a synergistic mediator of the pro-apoptotic effects conferred by JQ1 and PAN. This study proposes a candidate combination therapy of JQ1 and PAN to improve the therapeutic efficacy and worth further investigation in HNSCC.
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