Pathology, research and practice · 2025
Targeting CDH11 with celecoxib and derivatives to suppress esophageal squamous cell carcinoma proliferation and invasion.
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Xiao Lin, Yang Bingbing, Zhou Yijuan, Zhang Jiarui, Zhang Xiaoyan, Yang Wanjing, Sun Minjing, Li Mengmeng, Zhao Xueyan, Tian Fang
Аннотация
BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is a highly aggressive malignancy with limited therapeutic options. Cadherin-11 (CDH11) has been implicated in tumor progression, but its role in ESCC remains unclear.
METHODS: CDH11 expression was analyzed in ESCC tissues and cell lines. Functional assays (proliferation, migration, invasion) and xenograft models were employed to assess CDH11's role. Celecoxib and its derivative 2,5-dimethyl celecoxib (DMC) were evaluated as CDH11-targeted inhibitors.
RESULTS: CDH11 was overexpressed in ESCC tissues and correlated with lymph node metastasis and poor prognosis. Knockdown of CDH11 suppressed ESCC proliferation and invasion (P < 0.05), while overexpression exacerbated these phenotypes. Celecoxib and DMC directly bound CDH11 and inhibited ESCC growth in vitro and in vivo (IC50: 21.61-43.34 μM). Mechanistically, CDH11 knockdown attenuated JAK-STAT3 and AKT signaling.
CONCLUSION: CDH11 is a novel therapeutic target in ESCC, and its inhibition by celecoxib/DMC offers a promising strategy for ESCC treatment.
METHODS: CDH11 expression was analyzed in ESCC tissues and cell lines. Functional assays (proliferation, migration, invasion) and xenograft models were employed to assess CDH11's role. Celecoxib and its derivative 2,5-dimethyl celecoxib (DMC) were evaluated as CDH11-targeted inhibitors.
RESULTS: CDH11 was overexpressed in ESCC tissues and correlated with lymph node metastasis and poor prognosis. Knockdown of CDH11 suppressed ESCC proliferation and invasion (P < 0.05), while overexpression exacerbated these phenotypes. Celecoxib and DMC directly bound CDH11 and inhibited ESCC growth in vitro and in vivo (IC50: 21.61-43.34 μM). Mechanistically, CDH11 knockdown attenuated JAK-STAT3 and AKT signaling.
CONCLUSION: CDH11 is a novel therapeutic target in ESCC, and its inhibition by celecoxib/DMC offers a promising strategy for ESCC treatment.
Предметные рубрики MeSH
HumansCelecoxibCell ProliferationEsophageal NeoplasmsCadherinsAnimalsEsophageal Squamous Cell CarcinomaNeoplasm InvasivenessFemaleMaleCell MovementCell Line, TumorMiceMiddle AgedMice, NudeXenograft Model Antitumor AssaysSignal TransductionCyclooxygenase 2 InhibitorsMice, Inbred BALB CPyrazolesSulfonamides