Oops, you're using an old version of your browser so some of the features on this page may not be displaying properly.

MINIMAL Requirements: Google Chrome 24+Mozilla Firefox 20+Internet Explorer 11Opera 15–18Apple Safari 7SeaMonkey 2.15-2.23

Poster Display session 1

5616 - The effect of cortisol on methylation patterns in breast cancer cell lines

Date

28 Sep 2019

Session

Poster Display session 1

Topics

Basic Science

Tumour Site

Presenters

Haya Intabli

Citation

Annals of Oncology (2019) 30 (suppl_5): v1-v24. 10.1093/annonc/mdz238

Authors

H. Intabli1, M.S. Flint2, A. Qattan3, M. Allen2, M. Yeoman1

Author affiliations

  • 1 Pharmacy And Biomolecular Sciences, University of Brighton - Moulsecoomb campus, BN2 4GJ - Brighton/GB
  • 2 Pharmacy And Biomolecular Sciences, University of Brighton-Moulsecoomb campus, BN2 4GJ - Brighton/GB
  • 3 Molecular Oncology, King Faisal Specialist Hospital and Research Center, 11211 - Riyadh/SA

Resources

Login to access the resources on OncologyPRO.

If you do not have an ESMO account, please create one for free.

Abstract 5616

Background

Epigenetic changes are highly responsive to environmental changes, including stress. The release of stress hormones; such as glucocorticoids, in response to stress have been shown to induce epigenetic modifications in neuronal cells. However, the role of glucocorticoids on epigenetic changes underlying important processes such as cell cycle regulation, apoptosis, and proliferation in breast cancer are not yet established. Furthermore, it is not known if cortisol can induce irreversible epigenetic changes on these cellular processes and whether these changes relate to the duration of the stress response. In this study, cortisol-induced epigenetic changes and the potential involvement of DNA methylation was assessed.

Methods

We analyzed the expression levels of maintenance DNA methyltrasferase (DNMT1) in MDA-MB-231, Hs-578T, MCF7, and T47D breast cancer cell lines by real-time PCR. We also used Qiagen Epitect Methyl ll Complete PCR array for Tumour Suppressor genes to analyse the level of methylation in 94 tumour suppressor genes. The methylation level on the Long Interspersed Nuclear Element (LINE-1) was used as surrogate marker for global DNA methylation.

Results

Our results show that cortisol significantly decreased the expression of DNMT1 in the triple negative cells lines MDA-MB-231 (p < 0.005), and Hs-578T (p < 0.05). We also showed that cortisol induced aberrant methylation characterised by loss of methylation on promoter regions of key tumour suppressor genes in MDA-MB-231 cells, such as DAPK1, MGMT, AKT1, CDKN1A, and ABL1 and hypomethylation of the global genome.

Conclusions

Taken together, cortisol induced aberrant methylation patterns which may have important implications on progression of the disease.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

Has not received any funding.

Disclosure

All authors have declared no conflicts of interest.

This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used.

For more detailed information on the cookies we use, please check our Privacy Policy.

Customise settings
  • Necessary cookies enable core functionality. The website cannot function properly without these cookies, and you can only disable them by changing your browser preferences.