TIPE1 inhibits the growth of Ewing’s sarcoma cells by suppressing Wnt/β-catenin signaling

• Zhichao Wang ^[1] ; Libin Sun ^[1] ; Shuaiyin Liu ^[1] ; Haitao Jiang ^[2]
  1. [1] Dalian Medical University

     Dalian Medical University

     China

     
  2. [2] Department of Orthopedics, The Affiliated Taizhou People’s Hospital of Nanjing Medical University, Taizhou, 225300, China
• Localización: Clinical & translational oncology, ISSN 1699-048X, Vol. 25, Nº. 5 (May), 2023, págs. 1332-1339
• Idioma: inglés
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• Resumen

  • Background Ewing’s sarcoma is the second most common bone and soft tissue malignancy in children and adolescents. Tumor necrosis factor-α-induced protein 8-like 1 (TIPE1) functions as a tumor suppressor in several cancers. Activation of Wnt/β-catenin signaling in subpopulations of tumor cells contributes to phenotypic heterogeneity and disease progression in Ewing’s sarcoma. The exact role of TIPE1 in Ewing’s sarcoma remains to be elucidated.

    Purpose This study aimed to assess the expression and function of TIPE1 in Ewing’s sarcoma.

    Methods TIPE1 expression in Ewing’s sarcoma cells was determined by qPCR and western blotting. Furthermore, the Ewing’s sarcoma cell line RD-ES was transfected with a lentivirus-based TIPE1 expression system to upregulate the expression of TIPE1. The Cell Counting Kit 8 was used to assess the effect of TIPE1 on cell proliferation. The effects of TIPE1 on cell migration and invasion was detected by Transwell assay. Flow cytometry was performed to detect apoptosis.

    Results Our results suggested lower TIPE1 expression in Ewing’s sarcoma cell lines compared with normal osseous cells. TIPE1 remarkably inhibited the growth and proliferation of Ewing’s sarcoma cell; TIPE1 also induced apoptosis and inhibited invasion in vitro. TIPE1 inhibited Ewing’s sarcoma growth, motility, and survival through regulation of Wnt/β-catenin signaling.

    Conclusions Our results demonstrated the anti-tumor function of TIPE1 in Ewing’s sarcoma and reveal a novel therapeutic target.