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Hypoxia modulates the stem cell population and induces EMT in the MCF-10A breast epithelial cell line

  • Authors:
    • Carl S. Daly
    • Arwa Flemban
    • Mai Shafei
    • Myra E. Conway
    • David Qualtrough
    • Sarah J. Dean
  • View Affiliations / Copyright

    Affiliations: Department of Applied Sciences, Faculty of Health and Applied Sciences, University of West of England, Bristol, BS16 1QY, UK
    Copyright: © Daly et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 483-490
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    Published online on: December 1, 2017
       https://doi.org/10.3892/or.2017.6125
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Abstract

A common feature among pre-malignant lesions is the induction of hypoxia through increased cell propagation and reduced access to blood flow. Hypoxia in breast cancer has been associated with poor patient prognosis, resistance to chemotherapy and increased metastasis. Although hypoxia has been correlated with factors associated with the latter stages of cancer progression, it is not well documented how hypoxia influences cells in the earliest stages of transformation. Using the immortalized MCF-10A breast epithelial cell line, we used hypoxic culture conditions to mimic reduced O2 levels found within early pre-malignant lesions and assessed various cellular parameters. In this non-transformed mammary cell line, O2 deprivation led to some changes not immediately associated with cancer progression, such as decreased proliferation, cell cycle arrest and increased apoptosis. In contrast, hypoxia did induce other changes more consistent with an increased metastatic potential. A rise in the CD44+CD24-/low-labeled cell sub-population along with increased colony forming capability indicated an expanded stem cell population. Hypoxia also induced cellular and molecular changes consistent with an epithelial-to-mesenchymal transition (EMT). Furthermore, these cells now exhibited increased migratory and invasive abilities. These results underscore the contribution of the hypoxic tumour microenvironment in cancer progression and dissemination.
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Copy and paste a formatted citation
Spandidos Publications style
Daly CS, Flemban A, Shafei M, Conway ME, Qualtrough D and Dean SJ: Hypoxia modulates the stem cell population and induces EMT in the MCF-10A breast epithelial cell line. Oncol Rep 39: 483-490, 2018.
APA
Daly, C.S., Flemban, A., Shafei, M., Conway, M.E., Qualtrough, D., & Dean, S.J. (2018). Hypoxia modulates the stem cell population and induces EMT in the MCF-10A breast epithelial cell line. Oncology Reports, 39, 483-490. https://doi.org/10.3892/or.2017.6125
MLA
Daly, C. S., Flemban, A., Shafei, M., Conway, M. E., Qualtrough, D., Dean, S. J."Hypoxia modulates the stem cell population and induces EMT in the MCF-10A breast epithelial cell line". Oncology Reports 39.2 (2018): 483-490.
Chicago
Daly, C. S., Flemban, A., Shafei, M., Conway, M. E., Qualtrough, D., Dean, S. J."Hypoxia modulates the stem cell population and induces EMT in the MCF-10A breast epithelial cell line". Oncology Reports 39, no. 2 (2018): 483-490. https://doi.org/10.3892/or.2017.6125
Copy and paste a formatted citation
x
Spandidos Publications style
Daly CS, Flemban A, Shafei M, Conway ME, Qualtrough D and Dean SJ: Hypoxia modulates the stem cell population and induces EMT in the MCF-10A breast epithelial cell line. Oncol Rep 39: 483-490, 2018.
APA
Daly, C.S., Flemban, A., Shafei, M., Conway, M.E., Qualtrough, D., & Dean, S.J. (2018). Hypoxia modulates the stem cell population and induces EMT in the MCF-10A breast epithelial cell line. Oncology Reports, 39, 483-490. https://doi.org/10.3892/or.2017.6125
MLA
Daly, C. S., Flemban, A., Shafei, M., Conway, M. E., Qualtrough, D., Dean, S. J."Hypoxia modulates the stem cell population and induces EMT in the MCF-10A breast epithelial cell line". Oncology Reports 39.2 (2018): 483-490.
Chicago
Daly, C. S., Flemban, A., Shafei, M., Conway, M. E., Qualtrough, D., Dean, S. J."Hypoxia modulates the stem cell population and induces EMT in the MCF-10A breast epithelial cell line". Oncology Reports 39, no. 2 (2018): 483-490. https://doi.org/10.3892/or.2017.6125
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