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Article

SRPX and HMCN1 regulate cancer‑associated fibroblasts to promote the invasiveness of ovarian carcinoma

  • Authors:
    • Chao Lien Liu
    • Hung Wei Pan
    • Pao Ling Torng
    • Ming Huei Fan
    • Tsui Lien Mao
  • View Affiliations / Copyright

    Affiliations: School of Medical Laboratory Science and Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan, R.O.C., Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung 81362, Taiwan, R.O.C., Department of Obstetrics and Gynecology, National Taiwan University Hospital, Hsin‑Chu Branch, Hsinchu 30059, Taiwan, R.O.C., Department of Pathology, College of Medicine, National Taiwan University, Taipei 10002, Taiwan, R.O.C.
  • Pages: 2706-2715
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    Published online on: October 17, 2019
       https://doi.org/10.3892/or.2019.7379
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Abstract

Cancer‑associated fibroblasts (CAFs) are known to be essential in cancer initiation and development. However, the role of CAFs in promoting ovarian cancer (OC) invasion remains to be fully elucidated. To address this in the present study, 49 clinical OC specimens were used to evaluate the roles of CAFs in promoting ovarian tumor migration and invasion and disease progression. It was found that the sushi repeat‑containing protein, X‑linked (SRPX) and hemicentin 1 (HMCN1) genes were significantly upregulated in CAFs from high‑grade serous carcinoma (HGSC) and clear cell carcinoma (CCC) samples, the two major histological types of OC with frequently poor patient survival rates. The short hairpin (sh)RNA‑mediated silencing of SRPX and HMCN1 in fibroblasts significantly suppressed the Transwell invasive activities of OC cells. Further experiments showed that SRPX and HMCN1 regulated the invasiveness of OC via the Ras homology family member A (RhoA) signaling pathway in fibroblasts. Therefore, the findings of the present study suggest that targeting the CAF genes, SRPX and HMCN1, can inhibit OC migration and invasion. These data highlight the importance of CAF‑OC crosstalk signaling in cancer invasion and demonstrate the potential for improved efficacy of OC treatment by targeting CAF‑SRPX/HMCN1.
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Copy and paste a formatted citation
Spandidos Publications style
Liu CL, Pan HW, Torng PL, Fan MH and Mao TL: SRPX and HMCN1 regulate cancer‑associated fibroblasts to promote the invasiveness of ovarian carcinoma. Oncol Rep 42: 2706-2715, 2019.
APA
Liu, C.L., Pan, H.W., Torng, P.L., Fan, M.H., & Mao, T.L. (2019). SRPX and HMCN1 regulate cancer‑associated fibroblasts to promote the invasiveness of ovarian carcinoma. Oncology Reports, 42, 2706-2715. https://doi.org/10.3892/or.2019.7379
MLA
Liu, C. L., Pan, H. W., Torng, P. L., Fan, M. H., Mao, T. L."SRPX and HMCN1 regulate cancer‑associated fibroblasts to promote the invasiveness of ovarian carcinoma". Oncology Reports 42.6 (2019): 2706-2715.
Chicago
Liu, C. L., Pan, H. W., Torng, P. L., Fan, M. H., Mao, T. L."SRPX and HMCN1 regulate cancer‑associated fibroblasts to promote the invasiveness of ovarian carcinoma". Oncology Reports 42, no. 6 (2019): 2706-2715. https://doi.org/10.3892/or.2019.7379
Copy and paste a formatted citation
x
Spandidos Publications style
Liu CL, Pan HW, Torng PL, Fan MH and Mao TL: SRPX and HMCN1 regulate cancer‑associated fibroblasts to promote the invasiveness of ovarian carcinoma. Oncol Rep 42: 2706-2715, 2019.
APA
Liu, C.L., Pan, H.W., Torng, P.L., Fan, M.H., & Mao, T.L. (2019). SRPX and HMCN1 regulate cancer‑associated fibroblasts to promote the invasiveness of ovarian carcinoma. Oncology Reports, 42, 2706-2715. https://doi.org/10.3892/or.2019.7379
MLA
Liu, C. L., Pan, H. W., Torng, P. L., Fan, M. H., Mao, T. L."SRPX and HMCN1 regulate cancer‑associated fibroblasts to promote the invasiveness of ovarian carcinoma". Oncology Reports 42.6 (2019): 2706-2715.
Chicago
Liu, C. L., Pan, H. W., Torng, P. L., Fan, M. H., Mao, T. L."SRPX and HMCN1 regulate cancer‑associated fibroblasts to promote the invasiveness of ovarian carcinoma". Oncology Reports 42, no. 6 (2019): 2706-2715. https://doi.org/10.3892/or.2019.7379
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