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Article Open Access

Knockdown of ribosomal protein S15A inhibits human kidney cancer cell growth in vitro and in vivo

  • Authors:
    • Jiayu Liang
    • Zhihong Liu
    • Zijun Zou
    • Xiangxiu Wang
    • Yongquan Tang
    • Chuan Zhou
    • Kan Wu
    • Fuxun Zhang
    • Yiping Lu
  • View Affiliations / Copyright

    Affiliations: Department of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China, Core Facility, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China
    Copyright: © Liang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1117-1127
    |
    Published online on: December 12, 2018
       https://doi.org/10.3892/mmr.2018.9751
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Abstract

Ribosomal protein S15A (RPS15A), a member of the ribosomal protein gene family, was demonstrated to be closely associated with tumorigenesis in multiple human malignancies. Nevertheless, the role of RPS15A in the progression of renal cell carcinoma (RCC) remains unknown. In the present study, by comparing the publicly available data from RCC tissues and reverse transcription‑quantitative polymerase chain reaction results, it was identified that RPS15A was upregulated in RCC tissues and cell lines (P<0.001). Notably, knockdown of RPS15A suppressed 786‑O cell proliferation (P<0.001) and promoted its apoptosis/necrotic (P=0.0001) in vitro. Additionally, tumour formation and growth of transfected 786‑O cells were observed to be restrained in a mouse model (P<0.05). Subsequent to analysing the microarray data, 747 genes were differentially expressed in the RPS15A‑knockdown 786‑O cells. The enriched canonical pathways, diseases and functions of differentially expressed genes, and the interactive network of RPS15A in RCC were successfully constructed by ingenuity pathway analysis. Overall, the present results provided a preliminary experimental basis for RPS15A as a novel oncogene and potential therapeutic target in RCC.
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Copy and paste a formatted citation
Spandidos Publications style
Liang J, Liu Z, Zou Z, Wang X, Tang Y, Zhou C, Wu K, Zhang F and Lu Y: Knockdown of ribosomal protein S15A inhibits human kidney cancer cell growth in vitro and in vivo. Mol Med Rep 19: 1117-1127, 2019.
APA
Liang, J., Liu, Z., Zou, Z., Wang, X., Tang, Y., Zhou, C. ... Lu, Y. (2019). Knockdown of ribosomal protein S15A inhibits human kidney cancer cell growth in vitro and in vivo. Molecular Medicine Reports, 19, 1117-1127. https://doi.org/10.3892/mmr.2018.9751
MLA
Liang, J., Liu, Z., Zou, Z., Wang, X., Tang, Y., Zhou, C., Wu, K., Zhang, F., Lu, Y."Knockdown of ribosomal protein S15A inhibits human kidney cancer cell growth in vitro and in vivo". Molecular Medicine Reports 19.2 (2019): 1117-1127.
Chicago
Liang, J., Liu, Z., Zou, Z., Wang, X., Tang, Y., Zhou, C., Wu, K., Zhang, F., Lu, Y."Knockdown of ribosomal protein S15A inhibits human kidney cancer cell growth in vitro and in vivo". Molecular Medicine Reports 19, no. 2 (2019): 1117-1127. https://doi.org/10.3892/mmr.2018.9751
Copy and paste a formatted citation
x
Spandidos Publications style
Liang J, Liu Z, Zou Z, Wang X, Tang Y, Zhou C, Wu K, Zhang F and Lu Y: Knockdown of ribosomal protein S15A inhibits human kidney cancer cell growth in vitro and in vivo. Mol Med Rep 19: 1117-1127, 2019.
APA
Liang, J., Liu, Z., Zou, Z., Wang, X., Tang, Y., Zhou, C. ... Lu, Y. (2019). Knockdown of ribosomal protein S15A inhibits human kidney cancer cell growth in vitro and in vivo. Molecular Medicine Reports, 19, 1117-1127. https://doi.org/10.3892/mmr.2018.9751
MLA
Liang, J., Liu, Z., Zou, Z., Wang, X., Tang, Y., Zhou, C., Wu, K., Zhang, F., Lu, Y."Knockdown of ribosomal protein S15A inhibits human kidney cancer cell growth in vitro and in vivo". Molecular Medicine Reports 19.2 (2019): 1117-1127.
Chicago
Liang, J., Liu, Z., Zou, Z., Wang, X., Tang, Y., Zhou, C., Wu, K., Zhang, F., Lu, Y."Knockdown of ribosomal protein S15A inhibits human kidney cancer cell growth in vitro and in vivo". Molecular Medicine Reports 19, no. 2 (2019): 1117-1127. https://doi.org/10.3892/mmr.2018.9751
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