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Article

RON alternative splicing regulation in primary ovarian cancer

  • Authors:
    • Sebastian Mayer
    • Marc Hirschfeld
    • Markus Jaeger
    • Susanne Pies
    • Severine Iborra
    • Thalia Erbes
    • Elmar Stickeler
  • View Affiliations / Copyright

    Affiliations: Department of Obstetrics and Gynecology, University Medical Center Freiburg, Freiburg, Germany
  • Pages: 423-430
    |
    Published online on: May 19, 2015
       https://doi.org/10.3892/or.2015.3995
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Abstract

The proto-oncogene recepteur d'origine nantais (RON, MST1R) and its alternatively spliced variants are involved in various tumor biological processes, such as cell motility, adhesion, proliferation, apoptosis and epithelial-to-mesenchymal transition (EMT). RON overexpression and the occurrence of specific alternatively spliced RON isoforms have been detected in ovarian cancer. In the present study, we evaluated the role and regulation of cancer-related RON splicing isoforms in primary ovarian cancer. Expression of RON variants (RONΔ165, RONΔ160) was determined in 45 primary ovarian cancer and 4 physiological ovarian tissue specimens by RT-PCR and western blot analysis. The results were correlated to clinicopathological parameters. Additionally, expression of splicing factors with known involvement in RON alternative splicing regulation was examined. Increased RON levels were detected in all tumor samples (p=0.001) without differences between the primary tumors and metastases. Alternative RON variants were present in the majority of tumor samples (39 of 45; 86.67%). Potential RONΔ165 occurred more often (82.22%) than potential RONΔ160 or RONΔ155 (24.40%). Several significant correlations of RON and splicing factor expression [e.g. ASF/SFRS1 (p=0.035)] were detected. Correlations of RON expression to clinicopathological parameters were not observed. Significant splicing factor interactions (e.g. SRp55/SRp75: p<0.001) were observed in tumor samples with alternative RON splicing. Our data demonstrated upregulated RON isoform expression and significant changes in splicing factor expression in primary ovarian cancer. These findings account for an essential regulatory interplay of splicing factor-driven alterations in the RON alternative splicing pattern with subsequent tumor biological consequences in ovarian cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Mayer S, Hirschfeld M, Jaeger M, Pies S, Iborra S, Erbes T and Stickeler E: RON alternative splicing regulation in primary ovarian cancer. Oncol Rep 34: 423-430, 2015.
APA
Mayer, S., Hirschfeld, M., Jaeger, M., Pies, S., Iborra, S., Erbes, T., & Stickeler, E. (2015). RON alternative splicing regulation in primary ovarian cancer. Oncology Reports, 34, 423-430. https://doi.org/10.3892/or.2015.3995
MLA
Mayer, S., Hirschfeld, M., Jaeger, M., Pies, S., Iborra, S., Erbes, T., Stickeler, E."RON alternative splicing regulation in primary ovarian cancer". Oncology Reports 34.1 (2015): 423-430.
Chicago
Mayer, S., Hirschfeld, M., Jaeger, M., Pies, S., Iborra, S., Erbes, T., Stickeler, E."RON alternative splicing regulation in primary ovarian cancer". Oncology Reports 34, no. 1 (2015): 423-430. https://doi.org/10.3892/or.2015.3995
Copy and paste a formatted citation
x
Spandidos Publications style
Mayer S, Hirschfeld M, Jaeger M, Pies S, Iborra S, Erbes T and Stickeler E: RON alternative splicing regulation in primary ovarian cancer. Oncol Rep 34: 423-430, 2015.
APA
Mayer, S., Hirschfeld, M., Jaeger, M., Pies, S., Iborra, S., Erbes, T., & Stickeler, E. (2015). RON alternative splicing regulation in primary ovarian cancer. Oncology Reports, 34, 423-430. https://doi.org/10.3892/or.2015.3995
MLA
Mayer, S., Hirschfeld, M., Jaeger, M., Pies, S., Iborra, S., Erbes, T., Stickeler, E."RON alternative splicing regulation in primary ovarian cancer". Oncology Reports 34.1 (2015): 423-430.
Chicago
Mayer, S., Hirschfeld, M., Jaeger, M., Pies, S., Iborra, S., Erbes, T., Stickeler, E."RON alternative splicing regulation in primary ovarian cancer". Oncology Reports 34, no. 1 (2015): 423-430. https://doi.org/10.3892/or.2015.3995
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