Skip to main content
Log in

Association of miR-21 and miR-155 with regulation of 15-HPGD mRNA in human breast cancer cells

  • Published:
Biochemistry (Moscow) Supplement Series B: Biomedical Chemistry Aims and scope Submit manuscript

Abstract

Breast cancer (BC) is the most common form of cancer, leading to high mortality rates among women worldwide. In this study we have analyzed mRNA expression of 15-hydroxy-prostaglandin-dehydrogenases (15-HPGD), cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) and miRNAs (miR-21, miR-155) in three cell lines of estrogen-positive human breast carcinomas (MCF-7, BT-474, ZR-75-1). Results of three independent experiments have demonstrated significantly higher levels of COX-2 and COX-1 mRNAs in the cell line ZR-75-1 cells than in MCF-7 and BT-474 cells. mRNA levels of total 15-HPGD and functional-15-HPGD were lower in BT-474 than in MCF-7 and in ZR-75-1 cells. Synthesis of the 15-HPGD enzyme in BT-474 cells was blocked at the level of nuclear processing of an immature pre-mRNA. High expression of miR-21 was detected in all the tumor cell lines (MCF-7, ZR-75-1 and BT-474). In the breast cancer cell lines, the expression level of miR-155 was significantly lower than that of miR-21. Correlations have been found between dysregulation of miR-21, miR-155 and mRNA levels of 15-HPGD, COX-1, COX-2. The results obtained in this study showed that miR-21 and miR-155 regulate activity of several genes in the tumor cell and on some genes they exhibited a cumulative effect. Based on these results, we concluded that the miR-21 and miR-155 inhibit activity of the tumor suppressor gene 15-HPGD and induce a potential oncogene COX-2, which contributes to malignancy and metastasis of breast cancer cells.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

References

  1. Liu, G., Friggeri, A, Yang, Y., and Liu, G., J. Exp. Med., 2010, vol. 207, pp. 1589–1597.

    CAS  Google Scholar 

  2. Andrieu, N.A., Motiño, O., and Mayoral, R., PLoS One, 2012, vol. 7, e50935.

    Article  Google Scholar 

  3. Song, N.Y., Kim, D.H., and Kim, E.H., Chem. Res. Toxicol., 2011, vol. 24, pp. 1231–1241.

    CAS  Google Scholar 

  4. Yan, M., Rerko, R.M., and Platzer, P., Proc. Natl. Acad. Sci. USA, 2004, vol. 101, pp. 17468–17473.

    CAS  Google Scholar 

  5. Walker, J.D., Sehgal, I., and Kousoulas, K.G., J. Virol., 2011, vol. 85, pp. 7363–7371.

    CAS  Google Scholar 

  6. Ensor, C.M. and Tai, H.H., J. Lipid Mediat. Cell Signal., 1995, vol. 12, pp. 313–319.

    CAS  Google Scholar 

  7. Yan, L.-X., Huang, X.-F., and Shao, Q., RNA, 2008, vol. 14, pp. 2348–2360.

    Article  CAS  Google Scholar 

  8. Hanahan, D. and Weinberg, R.A., Cell, 2011, vol. 144, pp. 646–674.

    Article  CAS  Google Scholar 

  9. Roos, M.A., Bock, G.H. and Vries, J., J. Surg. Res., 2007, vol. 140, pp. 109–114.

    Google Scholar 

  10. Yiu, G.K. and Toker, A., J. Biol. Chem., 2006, vol. 281, pp. 12210–12217.

    CAS  Google Scholar 

  11. Singh, B., Berry, J.A., Shoher, B.S., and Lucci, A., J. Surgical Res., 2006, vol. 131, pp. 267–275.

    CAS  Google Scholar 

  12. Moore, A.E., Greenhough, A., Roberts, H.R., and Hicks, D.J., Carcinogenesis, 2009, vol. 30, no. 10, pp. 1796–1804.

    Article  CAS  Google Scholar 

  13. Lehtinen, L., Vainio, P., Wikman, H., Reemts, J., et al., J. Pathol., 2012, vol. 226, p. 674.

    CAS  Google Scholar 

  14. Vimalraj, S., Miranda, J.P., Ramyakrishna, B., Selvamurugan, N. Disease Markers, 2013, vol. 35, pp. 369–387.

    Article  CAS  Google Scholar 

  15. Piva, R., Spandidos, D.A., and Gambari, R., Int. J. Oncol., 2013, vol. 43, pp. 985–994.

    CAS  Google Scholar 

  16. Tang, J., Ahmad, A., and Sarkar, F.H., Int. J. Mol. Sci., 2012, vol. 13, pp. 13414–13437.

    CAS  Google Scholar 

  17. Zhu, S., Wu, H., Wu, F., et al., Cell Res., 2008, vol. 18, pp. 350–359.

    CAS  Google Scholar 

  18. Han, M., Liu, M., Wang, Y., et al., Mol. Cell Biochem., 2012, vol. 363, pp. 427–436.

    CAS  Google Scholar 

  19. Lu, Z., Ye, Y., Jiao, D., Qiao, J.I., Cui, S., and Liu, Z., Onc. Lett., 2012, vol. 4, pp. 1027–1032.

    CAS  Google Scholar 

  20. Sun, Y., Wang, M., Lin, G., Sun, S., Li, X., Qi, J., and Li, J., PLoS One, 2012, vol. 7, e47003.

    Article  CAS  Google Scholar 

  21. Strillaccia, A., Griffonia, C., Sansoneb, P., Paterinia, P., et al., Exp. Cell Res., 2009, vol. 315, pp. 1439–1447.

    Google Scholar 

  22. Dave, K., Oral Presentations University of South Carolina, 2012, Abstr., vol. 1, pp. 25–26. http://www.sc.edu/our/doc2012AbstractBook.pdf

    Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Z. N. Nikiforova.

Additional information

Original Russian Text © Z.N. Nikiforova, M.A.Taipov, I.A. Kudryavtsev, V.E. Shevchenko, 2015, published in Biomeditsinskaya Khimiya.

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Nikiforova, Z.N., Taipov, M.A., Kudryavtsev, I.A. et al. Association of miR-21 and miR-155 with regulation of 15-HPGD mRNA in human breast cancer cells. Biochem. Moscow Suppl. Ser. B 9, 159–165 (2015). https://doi.org/10.1134/S1990750815020110

Download citation

  • Received:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1134/S1990750815020110

Keywords

Navigation