Ayuda
Ir al contenido

Dialnet


Overexpression of dishevelled 2 is involved in tumor metastasis and is associated with poor prognosis in hepatocellular carcinoma

  • C. Zhang [1] ; C. Li [1] ; X. Chen [1] ; Y. Zhou [1] ; B. Yin [1] ; R. Ni [2] ; Y. Zhang [1] ; J. Liu [2]
    1. [1] Nantong University

      Nantong University

      China

    2. [2] Affiliated Hospital of Nantong University

      Affiliated Hospital of Nantong University

      China

  • Localización: Clinical & translational oncology, ISSN 1699-048X, Vol. 19, Nº. 12, 2017, págs. 1507-1517
  • Idioma: inglés
  • Texto completo no disponible (Saber más ...)
  • Resumen
    • Purpose Although hepatocellular carcinoma (HCC) is one of the most common malignant tumors, its molecular mechanism is still unknown. Dishevelled 2 (Dvl2) is one of the downstream targets of non-canonical Wnt signaling, which has been demonstrated to be of great importance in the progression of cancers. Nevertheless, the expression mechanisms and physiological significance of Dvl2 in HCC remain unclear.

      Methods Western blotting and immunohistochemistry were used to measure Dvl2 protein expression in HCC and adjacent normal tissues of 101 patients. Wound healing and transwell assays were used to determine cell migration and invasion.

      Results Dvl2 expression was upregulated in HCC tissues compared to the adjacent normal tissues. Moreover, its expression level was significantly correlated with histological grade (P = 0.042), metastasis (P = 0.005) and vein invasion (P = 0.009) in patients with HCC. Wound healing and transwell assays showed that knockdown of Dvl2 reduced cell migration and invasion in HepG2 cells. Finally, we confirmed that Dvl2 could regulate the migration and invasion of HCC cells by interacting with P62 in non-canonical Wnt signaling.

      Conclusions Our data showed that Dvl2 was overexpressed in HCC tissues and was also correlated with poor prognosis, suggesting that Dvl2 is a novel therapeutic target for HCC.


Fundación Dialnet

Dialnet Plus

  • Más información sobre Dialnet Plus

Opciones de compartir

Opciones de entorno