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Article

Kindlin‑2 promotes clear cell renal cell carcinoma progression through the Wnt signaling pathway

  • Authors:
    • Muhan Li
    • Xuelian Pei
    • Guoliang Wang
    • Jun Zhan
    • Juan Du
    • Hao Jiang
    • Yan Tang
    • Hongquan Zhang
    • Huiying He
  • View Affiliations / Copyright

    Affiliations: Key Laboratory of Carcinogenesis and Translational Research, Μinistry of Education, and State Key Laboratory of Natural and Biomimetic Drugs, Peking University Health Science Center, Beijing 100191, P.R. China, Department of Urology, Peking University Third Hospital, Beijing 100083, P.R. China
  • Pages: 1551-1560
    |
    Published online on: July 4, 2017
       https://doi.org/10.3892/or.2017.5789
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Abstract

Kindlin‑2 is an integrin-interacting, FERM-domain containing protein, which plays a critical role in tumor progression. However, the specific role of Kindlin‑2 in renal cell carcinoma (RCC) progression has not been described. In this study we investigated the role of Kindlin‑2 in progression of clear cell RCC (CCRCC), which is the most common RCC subtype, and its underlying mechanisms. Immunohistochemistry studies show that expression of Kindlin‑2 in CCRCC is positively correlated with tumor grade, and Kindlin‑2 expression in advanced CCRCC with lymph node metastasis was greater than in localized CCRCC. Kindlin‑2 expression in CCRCC tumor specimens is also correlated with short patient survival, but is not an independent prognostic factor. Kindlin‑2 promotes CCRCC cell migration and invasion in vitro, whereas knockdown of Kindlin‑2 inhibited cell migration and invasion. Knockdown of Kindlin‑2 also inhibits ACHN cell proliferation in vitro and tumorigenesis in vivo. Kindlin‑2 may be required for Wnt pathway activation which underlies the mechanisms of Kindlin‑2 promoting CCRCC progression. These findings demonstrate that expression of Kindlin‑2 is associated with tumor grade, lymph node metastasis and poor prognosis in CCRCC patients. Kindlin‑2 may regulate CCRCC progression through the Wnt signaling pathway, promoting CCRCC cell proliferation, migration and invasion.
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Copy and paste a formatted citation
Spandidos Publications style
Li M, Pei X, Wang G, Zhan J, Du J, Jiang H, Tang Y, Zhang H and He H: Kindlin‑2 promotes clear cell renal cell carcinoma progression through the Wnt signaling pathway. Oncol Rep 38: 1551-1560, 2017.
APA
Li, M., Pei, X., Wang, G., Zhan, J., Du, J., Jiang, H. ... He, H. (2017). Kindlin‑2 promotes clear cell renal cell carcinoma progression through the Wnt signaling pathway. Oncology Reports, 38, 1551-1560. https://doi.org/10.3892/or.2017.5789
MLA
Li, M., Pei, X., Wang, G., Zhan, J., Du, J., Jiang, H., Tang, Y., Zhang, H., He, H."Kindlin‑2 promotes clear cell renal cell carcinoma progression through the Wnt signaling pathway". Oncology Reports 38.3 (2017): 1551-1560.
Chicago
Li, M., Pei, X., Wang, G., Zhan, J., Du, J., Jiang, H., Tang, Y., Zhang, H., He, H."Kindlin‑2 promotes clear cell renal cell carcinoma progression through the Wnt signaling pathway". Oncology Reports 38, no. 3 (2017): 1551-1560. https://doi.org/10.3892/or.2017.5789
Copy and paste a formatted citation
x
Spandidos Publications style
Li M, Pei X, Wang G, Zhan J, Du J, Jiang H, Tang Y, Zhang H and He H: Kindlin‑2 promotes clear cell renal cell carcinoma progression through the Wnt signaling pathway. Oncol Rep 38: 1551-1560, 2017.
APA
Li, M., Pei, X., Wang, G., Zhan, J., Du, J., Jiang, H. ... He, H. (2017). Kindlin‑2 promotes clear cell renal cell carcinoma progression through the Wnt signaling pathway. Oncology Reports, 38, 1551-1560. https://doi.org/10.3892/or.2017.5789
MLA
Li, M., Pei, X., Wang, G., Zhan, J., Du, J., Jiang, H., Tang, Y., Zhang, H., He, H."Kindlin‑2 promotes clear cell renal cell carcinoma progression through the Wnt signaling pathway". Oncology Reports 38.3 (2017): 1551-1560.
Chicago
Li, M., Pei, X., Wang, G., Zhan, J., Du, J., Jiang, H., Tang, Y., Zhang, H., He, H."Kindlin‑2 promotes clear cell renal cell carcinoma progression through the Wnt signaling pathway". Oncology Reports 38, no. 3 (2017): 1551-1560. https://doi.org/10.3892/or.2017.5789
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