ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2026
Overexpression of cat eye syndrome chromosome region, candidate 2 in esophageal squamous carcinoma cell promotes tumor aggressiveness by facilitating NF-κB signaling and inhibition of p53-associated apoptosis.
Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 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
purposeA chromatin remodeling-related gene, cat eye syndrome chromosome region, candidate 2 (CECR2) was identified as candidate gene associated with aggressive phenotypes of esophageal squamous cell carcinoma (ESCC) in a transcriptome analysis. Here, we aimed to elucidate its role and potential for clinical application.
methodsWe evaluated ESCC cell lines modulating CECR2 expression in vitro. Signaling analysis and inhibitor experiments were conducted to reveal its potential mechanism. Mouse subcutaneous models were established to confirm the effect of knockdown and inhibitor. Expressions of CECR2 on mRNA level were analyzed by qPCR and protein level by TMA, respectively, in two cohorts.
resultsCECR2 was significantly upregulated in cancer tissue compared to normal tissue. CECR2 knockdown suppressed metastasis-related biological functions of ESCC cells and increased the sensitivity to principal anticancer reagents for treatment of ESCC, 5-FU and cisplatin. In addition, forced overexpression of CECR2 enhanced proliferation of low-CECR2-expressed cell line. Mechanistically, CECR2 upregulates NF-κB signaling, downregulates acetylated p53 expressions, and activates AKT signaling to enhance NF-κB signaling. Pharmacological inhibition of CECR2 by NVS-CECR2-1 induced cell apoptosis. In mouse subcutaneous models, permanent knockdown mediated by shCECR2 significantly inhibited tumor growth compared to shControl group; tumor growth was inhibited by a continual cycle of intraperitoneal administration of NVS-CECR2-1 compared to PBS only group. Analysis of two cohorts both demonstrated a significant association between high CECR2 mRNA/protein expression levels and poor prognosis.
conclusionUpregulation of CECR2 in ESCC promotes tumor aggressiveness and may serve as a potential therapeutic target for the treatment of ESCC.
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