ArticleFrontiers in pharmacology2026
Preclinical evaluation of JQ1 in esophageal squamous cell carcinoma: growth and migration suppression with BRD4-associated DNA damage and apoptotic signaling.
Article in Frontiers in pharmacology, 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
Background: Esophageal squamous cell carcinoma (ESCC) is an aggressive malignancy with limited therapeutic options. Bromodomain-containing protein 4 (BRD4), a BET family epigenetic reader, regulates oncogenic transcription and may represent a pharmacological vulnerability in ESCC. This study evaluated the pharmacological effects of the BET inhibitor JQ1 in ESCC models, with particular attention to cell migration under non-cytotoxic conditions and BRD4-associated stress signaling. Methods: The effects of JQ1 were examined in ESCC cell lines and in a KYSE150 subcutaneous xenograft model established in BALB/c nude mice. Cell viability was assessed by CCK-8 assays at 24, 48, and 72 h. Wound healing and Transwell assays were performed using cell-line-specific low concentrations of JQ1 that did not significantly reduce cell viability during the 24 h assay period, as confirmed by parallel viability controls. Cell-cycle distribution and apoptosis were analyzed by flow cytometry. Western blotting, immunofluorescence staining, qRT-PCR, and alkaline comet assay were used to assess BRD4-related signaling, apoptosis-associated proteins, γ-H2AX accumulation, and DNA strand breaks. Results: JQ1 reduced ESCC cell viability and clonogenic growth, induced G1-phase accumulation, and promoted apoptosis-associated changes. Under non-cytotoxic conditions, JQ1 reduced wound closure and Transwell migration in KYSE150, KYSE450, and ECA109 cells. Molecular analyses showed that JQ1 treatment was accompanied by decreased BRD4 expression, suppression of c-Myc/Cyclin D1-related signaling, increased p53 and Bax expression, reduced Bcl-2 expression, and elevated levels of cleaved PARP1 and cleaved Caspase-3. JQ1 also increased γ-H2AX accumulation and DNA strand breaks. Conclusion: JQ1 exhibited anti-proliferative, pro-apoptotic, and anti-migratory effects in preclinical ESCC models. These effects were accompanied by BRD4-related signaling changes, DNA damage-associated responses, and apoptosis-related molecular alterations. The findings support further investigation of BET/BRD4-associated pharmacological strategies in ESCC, while target-specific validation and expanded
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