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Xiaojia LIU, Qiqi ZHANG, Xiujuan LI, Zhiqiang YI, Zhiqiang ZHANG. SDC2 Promotes Malignant Progression of Esophageal Squamous Cell Carcinoma via the STAT3 Signaling Pathway[J]. Journal of Kunming Medical University.
Citation: Xiaojia LIU, Qiqi ZHANG, Xiujuan LI, Zhiqiang YI, Zhiqiang ZHANG. SDC2 Promotes Malignant Progression of Esophageal Squamous Cell Carcinoma via the STAT3 Signaling Pathway[J]. Journal of Kunming Medical University.

SDC2 Promotes Malignant Progression of Esophageal Squamous Cell Carcinoma via the STAT3 Signaling Pathway

  • Received Date: 2025-12-23
    Available Online: 2026-04-26
  • To investigate the positive expression of syndecan-2 (SDC2) in esophageal squamous cell carcinoma (ESCC), analyze its correlation with clinical prognosis and pathological parameters of ESCC patients, and explore the effects of SDC2 on the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of ESCC cells. To clarify its relationship with STAT3 signaling pathway. Methods:Immunohistochemistry was used to detect the expression of SDC2 in 120 ESCC tissues and 80 paired adjacent tissues. Chi-square test was used to analyze the correlation between SDC2 positive expression and clinicopathological parameters of patients. Kaplan-Meier method was used to evaluate its effect on prognosis. The ESCC cell model with stable knockdown and overexpression of SDC2 was constructed by lentivirus transfection. The effects of SDC2 on the malignant biological behavior and STAT3 pathway of ESCC cells were detected by CCK-8, clone formation, scratch test, Transwell test and Western blot. Results:The expression level of SDC2 in ESCC tissues was significantly higher than that in adjacent tissues (P < 0.05). The expression of SDC2 was significantly correlated with the pathological stage of patients (P < 0.05), and the overall survival of patients with high expression was shorter (P < 0.05). Knockdown of SDC2 inhibited the proliferation, migration and invasion of KYSE-150 cells, down-regulated the expression of Vimentin, Snail and p-STAT3Tyr705, and up-regulated the expression of E-cadherin (P < 0.05). Overexpression of SDC2 promoted the proliferation, migration and invasion of Eca-109 cells, up-regulated the expression of Vimentin, Snail and p-STAT3Tyr705, and down-regulated the expression of E-cadherin(P < 0.05). The application of STAT3 inhibitor Stattic in Eca-109 cells overexpressing SDC2 could significantly inhibit the phosphorylation level of STAT3(P < 0.05). Conclusion:SDC2 is highly expressed in ESCC, which is closely related to the clinicopathological stage and poor prognosis of patients. As a key downstream effector molecule, STAT3 drives cell proliferation, migration, invasion and EMT processes by activating the STAT3 signaling pathway.
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