Page 42 - SDIR5 Abstract book 21 12 2021.

POSTER PRESENTATIONS

P2

In Vitro Investigations of miR-33a Expression in Estrogen Receptor-Targeting Therapies in
Breast Cancer Cells

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3
1
2
Pelin Ozfiliz-Kilbas , Ozlem Sonmez , Pinar Obakan-Yerlikaya , Ajda Coker-Gurkan , Narcin Palavan-
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Unsal , Pinar Uysal-Onganer , and Elif Damla Arisan
1 Department of Molecular Biology and Genetics, Istanbul Kultur University, 34158 Istanbul, Turkey
2 Department of Biomedical Engineering, Biruni University, 34010 Istanbul, Turkey
3 Department of Molecular Biology and Genetics, Biruni University, 34010 Istanbul, Turkey
4 Department, Netkent Mediterranean Research and Science University, 38-44 Kyrenia
5 Cancer Research Group, School of Life Sciences, University of Westminster, London, UK
6 Institute of Biotechnology, Gebze Technical University, 41400 Gebze, Turkey

Background: Elevated levels of fatty acid production promote breast cancer's aggressive character and
reduces treatment efficacy. Regulatory microRNAs (miRNAs) on lipid production pathways, such as miR-
33a, may be able to enlighten the mechanism. In the current study, we aimed to elucidate the role of miR-
33a in MCF-7 and MDA-MB-231 breast cancer cells related to fatty acid mechanism in the treatment of
estrogen receptor (ER) activator (estradiol-17β, E2) and anti-estrogens (ICI 182,780, Fulvestrant, FUL).
Results: Treatment of MCF-7 cells with E2 and FUL did not cause a significant cell viability decrease at low
concentrations, whereas higher concentrations showed a suppressive effect on cell survival. We
determined miR-33a expression levels in MCF-7 and MDA-MB-231 breast cancer cells following E2 and FUL
treatment and observed that FUL treatment enhanced the miR-33a expression both in MCF-7 and MDA-
MB-231 cells. Considering the key regulator role of miR-33a on cholesterol mechanism, we investigated the
expression profile of fatty acid synthesis pathway members in miR-33a mimics or anti-miR-33a treated-
breast cancer cells. Conclusion: According to our results, the cellular expression level of miR-33a is critical
to understanding differential responses of breast cancer cells.

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