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Article

High miR-122 expression promotes malignant phenotypes in ccRCC by targeting occludin

  • Authors:
    • Kentaro Jingushi
    • Yuri Kashiwagi
    • Yuko Ueda
    • Kaori Kitae
    • Hiroaki Hase
    • Wataru Nakata
    • Kazutoshi Fujita
    • Motohide Uemura
    • Norio Nonomura
    • Kazutake Tsujikawa
  • View Affiliations / Copyright

    Affiliations: Laboratory of Molecular and Cellular Physiology, Graduate School of Pharmaceutical Sciences, Osaka University, Suita, Osaka 565-0871, Japan, Department of Urology, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan
  • Pages: 289-297
    |
    Published online on: May 22, 2017
       https://doi.org/10.3892/ijo.2017.4016
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Abstract

Renal cell carcinoma (RCC) is the most common neoplasm of the adult kidney, and clear cell RCC (ccRCC) represents its most common histological subtype. Although several studies have reported high expression of miR-122 in ccRCC, its physiological role remains unclear. To clarify the role of miR-122 in ccRCC, we compared miR-122 expression levels in non-cancerous tissue and ccRCC. Significant upregulation of miR-122 was observed in ccRCC specimens. Moreover, ccRCC patients with high miR-122 expression showed poor progression-free survival compared to those with low miR-122 expression. Overexpression of miR-122 using an miRNA mimic promoted proliferation, migration, and invasion activities of ccRCC cells. miR-122 directly targets occludin, a known component of tight junctions. Occludin knockdown promoted the cell migration activity but not proliferation or invasion activities of ccRCC cells. In human clinical specimens, miR-122 expression inversely correlated with occludin protein expression. These findings show that miR-122 is an oncomiR in ccRCC.
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Copy and paste a formatted citation
Spandidos Publications style
Jingushi K, Kashiwagi Y, Ueda Y, Kitae K, Hase H, Nakata W, Fujita K, Uemura M, Nonomura N, Tsujikawa K, Tsujikawa K, et al: High miR-122 expression promotes malignant phenotypes in ccRCC by targeting occludin. Int J Oncol 51: 289-297, 2017.
APA
Jingushi, K., Kashiwagi, Y., Ueda, Y., Kitae, K., Hase, H., Nakata, W. ... Tsujikawa, K. (2017). High miR-122 expression promotes malignant phenotypes in ccRCC by targeting occludin. International Journal of Oncology, 51, 289-297. https://doi.org/10.3892/ijo.2017.4016
MLA
Jingushi, K., Kashiwagi, Y., Ueda, Y., Kitae, K., Hase, H., Nakata, W., Fujita, K., Uemura, M., Nonomura, N., Tsujikawa, K."High miR-122 expression promotes malignant phenotypes in ccRCC by targeting occludin". International Journal of Oncology 51.1 (2017): 289-297.
Chicago
Jingushi, K., Kashiwagi, Y., Ueda, Y., Kitae, K., Hase, H., Nakata, W., Fujita, K., Uemura, M., Nonomura, N., Tsujikawa, K."High miR-122 expression promotes malignant phenotypes in ccRCC by targeting occludin". International Journal of Oncology 51, no. 1 (2017): 289-297. https://doi.org/10.3892/ijo.2017.4016
Copy and paste a formatted citation
x
Spandidos Publications style
Jingushi K, Kashiwagi Y, Ueda Y, Kitae K, Hase H, Nakata W, Fujita K, Uemura M, Nonomura N, Tsujikawa K, Tsujikawa K, et al: High miR-122 expression promotes malignant phenotypes in ccRCC by targeting occludin. Int J Oncol 51: 289-297, 2017.
APA
Jingushi, K., Kashiwagi, Y., Ueda, Y., Kitae, K., Hase, H., Nakata, W. ... Tsujikawa, K. (2017). High miR-122 expression promotes malignant phenotypes in ccRCC by targeting occludin. International Journal of Oncology, 51, 289-297. https://doi.org/10.3892/ijo.2017.4016
MLA
Jingushi, K., Kashiwagi, Y., Ueda, Y., Kitae, K., Hase, H., Nakata, W., Fujita, K., Uemura, M., Nonomura, N., Tsujikawa, K."High miR-122 expression promotes malignant phenotypes in ccRCC by targeting occludin". International Journal of Oncology 51.1 (2017): 289-297.
Chicago
Jingushi, K., Kashiwagi, Y., Ueda, Y., Kitae, K., Hase, H., Nakata, W., Fujita, K., Uemura, M., Nonomura, N., Tsujikawa, K."High miR-122 expression promotes malignant phenotypes in ccRCC by targeting occludin". International Journal of Oncology 51, no. 1 (2017): 289-297. https://doi.org/10.3892/ijo.2017.4016
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