2. Academic Validation
  3. Targeting CDH11 with celecoxib and derivatives to suppress esophageal squamous cell carcinoma proliferation and invasion

Targeting CDH11 with celecoxib and derivatives to suppress esophageal squamous cell carcinoma proliferation and invasion

  • Pathol Res Pract. 2025 Aug:272:156042. doi: 10.1016/j.prp.2025.156042.
Lin Xiao 1,  Bingbing Yang 2,  Yijuan Zhou 2,  Jiarui Zhang 2,  Xiaoyan Zhang 2,  Wanjing Yang 2,  Minjing Sun 1,  Mengmeng Li 1,  Xueyan Zhao 3,  Fang Tian 4
Affiliations

Affiliations

  • 1 Department of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450001, China.
  • 2 Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan 450001, China.
  • 3 Department of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450001, China. Electronic address: 15038354168@163.com.
  • 4 Department of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450001, China; Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan 450001, China; Department of Pathology and Forensic Medicine, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan 450001, China. Electronic address: tianfang418@163.com.
PMID: 40460640 DOI: 10.1016/j.prp.2025.156042
Abstract

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.

Keywords

2; 5-DiMethyl Celecoxib; Cadherin-11; Celecoxib; Esophageal squamous cell carcinoma.

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