Open Access

Cancer stem cell marker CD90 inhibits ovarian cancer formation via β3 integrin

  • Authors:
    • Wei-Ching Chen
    • Hui-Ping Hsu
    • Chung-Yen Li
    • Ya-Ju Yang
    • Yu-Hsuan Hung
    • Chien-Yu Cho
    • Chih-Yang Wang
    • Tzu-Yang Weng
    • Ming-Derg Lai
  • View Affiliations

  • Published online on: September 15, 2016     https://doi.org/10.3892/ijo.2016.3691
  • Pages: 1881-1889
  • Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Cancer stem cell (CSC) markers have been identified for CSC isolation and proposed as therapeutic targets in various types of cancers. CD90, one of the characterized markers in liver and gastric cancer, is shown to promote cancer formation. However, the underexpression level of CD90 in ovarian cancer cells and the evidence supporting the cellular mechanism have not been investigated. In the present study, we found that the DNA copy number of CD90 is correlated with mRNA expression in ovarian cancer tissue and the ovarian cancer patients with higher CD90 have good prognosis compared to the patients with lower CD90. Although the expression of CD90 in human ovarian cancer SKOV3 cells enhances the cell proliferation by MTT and anchorage-dependent growth assay, CD90 inhibits the anchorage-independent growth ability in vitro and tumor formation in vivo. CD90 overexpression suppresses the sphere-forming ability and ALDH activity and enhances the cell apoptosis, indicating that CD90 may reduce the cell growth by the properties of CSC and anoikis. Furthermore, CD90 reduces the expression of other CSC markers, including CD133 and CD24. The inhibition of CD133 is attenuated by the mutant CD90, which is replaced with RLE domain into RLD domain. Importantly, the CD90-regulated inhibition of CD133 expression, anchorage-independent growth and signal transduction of mTOR and AMPK are restored by the β3 integrin shRNA. Our results provide evidence that CD90 mediates the antitumor formation by interacting with β3 integrin, which provides new insight that can potentially be applied in the development of therapeutic strategies in ovarian cancer.
View Figures
View References

Related Articles

Journal Cover

November-2016
Volume 49 Issue 5

Print ISSN: 1019-6439
Online ISSN:1791-2423

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Chen W, Hsu H, Li C, Yang Y, Hung Y, Cho C, Wang C, Weng T and Lai M: Cancer stem cell marker CD90 inhibits ovarian cancer formation via β3 integrin. Int J Oncol 49: 1881-1889, 2016.
APA
Chen, W., Hsu, H., Li, C., Yang, Y., Hung, Y., Cho, C. ... Lai, M. (2016). Cancer stem cell marker CD90 inhibits ovarian cancer formation via β3 integrin. International Journal of Oncology, 49, 1881-1889. https://doi.org/10.3892/ijo.2016.3691
MLA
Chen, W., Hsu, H., Li, C., Yang, Y., Hung, Y., Cho, C., Wang, C., Weng, T., Lai, M."Cancer stem cell marker CD90 inhibits ovarian cancer formation via β3 integrin". International Journal of Oncology 49.5 (2016): 1881-1889.
Chicago
Chen, W., Hsu, H., Li, C., Yang, Y., Hung, Y., Cho, C., Wang, C., Weng, T., Lai, M."Cancer stem cell marker CD90 inhibits ovarian cancer formation via β3 integrin". International Journal of Oncology 49, no. 5 (2016): 1881-1889. https://doi.org/10.3892/ijo.2016.3691