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Article

R-spondin 2 promotes proliferation and migration via the Wnt/β-catenin pathway in human hepatocellular carcinoma

  • Authors:
    • Xinguang Yin
    • Huixing Yi
    • Linlin Wang
    • Wanxin Wu
    • Xiaojun Wu
    • Linghua Yu
  • View Affiliations / Copyright

    Affiliations: Centre for Gastroenterology and Hepatology, The First Affiliated Hospital of Jiaxing College, Jiaxing, Zhejiang 314001, P.R. China, Intensive Care Unit, The Second Affiliated Hospital of Zhejiang University, Hangzhou, Zhejiang 310009, P.R. China, Department of Basic Medicine Sciences, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310058, P.R. China, Deparment of Pathology, The First Affiliated Hospital of Jiaxing College, Jiaxing, Zhejiang 314001, P.R. China
  • Pages: 1757-1765
    |
    Published online on: June 7, 2017
       https://doi.org/10.3892/ol.2017.6339
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Abstract

Hepatocellular carcinoma (HCC) is a leading cause of malignant disease-associated mortality, particularly in China. The RSPO2 (R‑spondin 2) gene is evolutionarily conserved in vertebrates and is involved in developmental and physiological processes. Importantly, RSPO2 has been reported to be associated with colon cancer and potentiate the Wnt/β‑catenin signaling pathway. In the present study, enhanced expression of RSPO2 in HCC was observed using tissue microarray. Similarly, the expression level of RSPO2 was higher in HepG2, Huh7 and Hep3B cells but lower in Bel7404 and QGY7703 cells compared with human normal QSG7701 liver cells. Subsequently, gain‑of‑function studies indicated that RSPO2 promotes the proliferation and migration of QGY7703 cells based on lentivirus‑based gene delivery. Furthermore, it was revealed that p21 and leptin, rather than vascular endothelial growth factor‑A, are involved in the function of RSPO2 in QGY7703 cells. Particularly, the signal transducer and activator of transcription 3 (STAT3) and Wnt/β‑catenin signaling pathways are involved in this process. Overexpression of RSPO2 resulted in the elevated expression of phosphorylated STAT3, β‑catenin and c‑Myc. Therefore, the present study is beneficial to the understanding of RSPO2‑involved liver cancer transformation and drug discovery.
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Copy and paste a formatted citation
Spandidos Publications style
Yin X, Yi H, Wang L, Wu W, Wu X and Yu L: R-spondin 2 promotes proliferation and migration via the Wnt/β-catenin pathway in human hepatocellular carcinoma. Oncol Lett 14: 1757-1765, 2017.
APA
Yin, X., Yi, H., Wang, L., Wu, W., Wu, X., & Yu, L. (2017). R-spondin 2 promotes proliferation and migration via the Wnt/β-catenin pathway in human hepatocellular carcinoma. Oncology Letters, 14, 1757-1765. https://doi.org/10.3892/ol.2017.6339
MLA
Yin, X., Yi, H., Wang, L., Wu, W., Wu, X., Yu, L."R-spondin 2 promotes proliferation and migration via the Wnt/β-catenin pathway in human hepatocellular carcinoma". Oncology Letters 14.2 (2017): 1757-1765.
Chicago
Yin, X., Yi, H., Wang, L., Wu, W., Wu, X., Yu, L."R-spondin 2 promotes proliferation and migration via the Wnt/β-catenin pathway in human hepatocellular carcinoma". Oncology Letters 14, no. 2 (2017): 1757-1765. https://doi.org/10.3892/ol.2017.6339
Copy and paste a formatted citation
x
Spandidos Publications style
Yin X, Yi H, Wang L, Wu W, Wu X and Yu L: R-spondin 2 promotes proliferation and migration via the Wnt/β-catenin pathway in human hepatocellular carcinoma. Oncol Lett 14: 1757-1765, 2017.
APA
Yin, X., Yi, H., Wang, L., Wu, W., Wu, X., & Yu, L. (2017). R-spondin 2 promotes proliferation and migration via the Wnt/β-catenin pathway in human hepatocellular carcinoma. Oncology Letters, 14, 1757-1765. https://doi.org/10.3892/ol.2017.6339
MLA
Yin, X., Yi, H., Wang, L., Wu, W., Wu, X., Yu, L."R-spondin 2 promotes proliferation and migration via the Wnt/β-catenin pathway in human hepatocellular carcinoma". Oncology Letters 14.2 (2017): 1757-1765.
Chicago
Yin, X., Yi, H., Wang, L., Wu, W., Wu, X., Yu, L."R-spondin 2 promotes proliferation and migration via the Wnt/β-catenin pathway in human hepatocellular carcinoma". Oncology Letters 14, no. 2 (2017): 1757-1765. https://doi.org/10.3892/ol.2017.6339
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