Open Access

miR-195 inhibits cell proliferation and angiogenesis in human prostate cancer by downregulating PRR11 expression

Corrigendum in: /10.3892/or.2023.8507

  • Authors:
    • Chao Cai
    • Huichan He
    • Xiaolu Duan
    • Wenqi Wu
    • Zanlin Mai
    • Tao Zhang
    • Junhong Fan
    • Tuo Deng
    • Wen Zhong
    • Yongda Liu
    • Weide Zhong
    • Guohua Zeng
  • View Affiliations

  • Published online on: January 31, 2018     https://doi.org/10.3892/or.2018.6240
  • Pages: 1658-1670
  • Copyright: © Cai et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

hsa-miR-195-5p (miR-195) has been proven to be a critical regulator in the progression of prostate cancer (PCa). To identify additional targets and molecular functions of miR-195, we overexpressed miR-195 by transient oligonucleotide transfection in DU145 and LNCaP cells and examined the effects. RNA-based microarray and dual-luciferase assays were carried out to identify novel targets of miR-195, while in vitro functional assays, a subcutaneous xenograft model, tissue microarray (TMA) analysis and a cohort of publicly available data (Taylor cohort) were used to investigate the biological function and clinical value of miR-195 targeting. The results shown that miR-195 overexpression could markedly suppress cellular proliferation and tube formation compared with miR-negative control. The RNA-based microarray identified a total of 153 differentially regulated genes with fold changes of ≤|1.5|, including 138 (90.2%) downregulated and 15 (9.8%) upregulated genes. Among the downregulated genes, we found that proline-rich protein 11 (PRR11) combined with miR-195 expression (miR-195/PRR11) could be used as an independent predictor of the risk of biochemical recurrence in the Taylor cohort. Additionally, the dual-luciferase assay identified PRR11 as a novel target of miR-195, and the in vitro assays indicated that PRR11 abrogated the suppressive effects of miR-195 on cell proliferation, tube formation and cell cycling. Furthermore, the subcutaneous tumor xenograft model indicated that knockdown of PRR11 inhibited xenograft growth and angiogenesis, while the results of the TMA and Taylor cohort analyses collectively demonstrated that PRR11 expression was upregulated in aggressive tumors and is associated with poor clinical outcome. Taken together, these findings further illustrate the suppressive role of miR-195 in PCa, and indicate a novel role of PRR11 in PCa. Importantly, the newly identified miR-195/PRR11 axis may aid with identifying potential therapeutic targets in PCa.
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April-2018
Volume 39 Issue 4

Print ISSN: 1021-335X
Online ISSN:1791-2431

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Copy and paste a formatted citation
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Spandidos Publications style
Cai C, He H, Duan X, Wu W, Mai Z, Zhang T, Fan J, Deng T, Zhong W, Liu Y, Liu Y, et al: miR-195 inhibits cell proliferation and angiogenesis in human prostate cancer by downregulating PRR11 expression Corrigendum in /10.3892/or.2023.8507. Oncol Rep 39: 1658-1670, 2018
APA
Cai, C., He, H., Duan, X., Wu, W., Mai, Z., Zhang, T. ... Zeng, G. (2018). miR-195 inhibits cell proliferation and angiogenesis in human prostate cancer by downregulating PRR11 expression Corrigendum in /10.3892/or.2023.8507. Oncology Reports, 39, 1658-1670. https://doi.org/10.3892/or.2018.6240
MLA
Cai, C., He, H., Duan, X., Wu, W., Mai, Z., Zhang, T., Fan, J., Deng, T., Zhong, W., Liu, Y., Zhong, W., Zeng, G."miR-195 inhibits cell proliferation and angiogenesis in human prostate cancer by downregulating PRR11 expression Corrigendum in /10.3892/or.2023.8507". Oncology Reports 39.4 (2018): 1658-1670.
Chicago
Cai, C., He, H., Duan, X., Wu, W., Mai, Z., Zhang, T., Fan, J., Deng, T., Zhong, W., Liu, Y., Zhong, W., Zeng, G."miR-195 inhibits cell proliferation and angiogenesis in human prostate cancer by downregulating PRR11 expression Corrigendum in /10.3892/or.2023.8507". Oncology Reports 39, no. 4 (2018): 1658-1670. https://doi.org/10.3892/or.2018.6240