In Vitro Investigations of miR-33a Expression in Estrogen Receptor-Targeting Therapies in Breast Cancer Cells
(1) Background: Increased fatty acid synthesis leads to the aggressive phenotype of breast cancer and renders efficiency of therapeutics. Regulatory microRNAs (miRNAs) on lipid biosynthesis pathways as miR-33a have potential to clarify the exact mechanism. (2) Methods: We determined miR-33a expressi...
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| Format: | Article |
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MDPI AG
2021-10-01
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| Series: | Cancers |
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| Online Access: | https://www.mdpi.com/2072-6694/13/21/5322 |
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| author | Pelin Ozfiliz-Kilbas Ozlem Sonmez Pinar Obakan-Yerlikaya Ajda Coker-Gurkan Narcin Palavan-Ünsal Pinar Uysal-Onganer Elif Damla Arisan |
| author_facet | Pelin Ozfiliz-Kilbas Ozlem Sonmez Pinar Obakan-Yerlikaya Ajda Coker-Gurkan Narcin Palavan-Ünsal Pinar Uysal-Onganer Elif Damla Arisan |
| author_sort | Pelin Ozfiliz-Kilbas |
| collection | DOAJ |
| description | (1) Background: Increased fatty acid synthesis leads to the aggressive phenotype of breast cancer and renders efficiency of therapeutics. Regulatory microRNAs (miRNAs) on lipid biosynthesis pathways as miR-33a have potential to clarify the exact mechanism. (2) Methods: We determined miR-33a expression levels following exposure of MCF-7 and MDA-MB-231 breast cancer cells to estrogen receptor (ER) activator (estradiol-17β, E2) or anti-estrogens (ICI 182,780, Fulvestrant, FUL) at non-cytotoxic concentrations. We related miR-33a expression levels in the cells to cellular lipid biosynthesis-related pathways through immunoblotting. (3) Results: miR-33a mimic treatment led to significantly downregulation of fatty acid synthase (FASN) in MCF-7 cells but not in MDA-MB-231 cells in the presence of estradiol-17β (E2) or Fulvestrant (FUL). In contrast to the miR-33a inhibitor effect, miR-33a mimic co-transfection with E2 or FUL led to diminished AMP-activated protein kinase α (AMPKα) activity in MCF-7 cells. E2 increases FASN levels in MDA-MB-231 cells regardless of miR-33a cellular levels. miR-33a inhibitor co-treatment suppressed E2-mediated AMPKα activity in MDA-MB-231 cells. (4) Conclusions: The cellular expression levels of miR-33a are critical to understanding differential responses which include cellular energy sensors such as AMPKα activation status in breast cancer cells. |
| first_indexed | 2024-03-10T06:05:33Z |
| format | Article |
| id | doaj.art-68b7df5e3f8c498a9e8a126c6d8ae068 |
| institution | Directory Open Access Journal |
| issn | 2072-6694 |
| language | English |
| last_indexed | 2024-03-10T06:05:33Z |
| publishDate | 2021-10-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cancers |
| spelling | doaj.art-68b7df5e3f8c498a9e8a126c6d8ae0682023-11-22T20:33:33ZengMDPI AGCancers2072-66942021-10-011321532210.3390/cancers13215322In Vitro Investigations of miR-33a Expression in Estrogen Receptor-Targeting Therapies in Breast Cancer CellsPelin Ozfiliz-Kilbas0Ozlem Sonmez1Pinar Obakan-Yerlikaya2Ajda Coker-Gurkan3Narcin Palavan-Ünsal4Pinar Uysal-Onganer5Elif Damla Arisan6Department of Molecular Biology and Genetics, Istanbul Kultur University, Istanbul 34158, TurkeyDepartment of Molecular Biology and Genetics, Istanbul Kultur University, Istanbul 34158, TurkeyDepartment of Biomedical Engineering, Biruni University, Istanbul 34010, TurkeyDepartment of Molecular Biology and Genetics, Biruni University, Istanbul 34010, TurkeyDepartment of Engineering, Netkent Mediterranean Research and Science University, 38-44 Kyrenia, Macka 99300, TurkeyCancer Research Group, School of Life Sciences, University of Westminster, London W1W 6UW, UKInstitute of Biotechnology, Gebze Technical University, Gebze 41400, Turkey(1) Background: Increased fatty acid synthesis leads to the aggressive phenotype of breast cancer and renders efficiency of therapeutics. Regulatory microRNAs (miRNAs) on lipid biosynthesis pathways as miR-33a have potential to clarify the exact mechanism. (2) Methods: We determined miR-33a expression levels following exposure of MCF-7 and MDA-MB-231 breast cancer cells to estrogen receptor (ER) activator (estradiol-17β, E2) or anti-estrogens (ICI 182,780, Fulvestrant, FUL) at non-cytotoxic concentrations. We related miR-33a expression levels in the cells to cellular lipid biosynthesis-related pathways through immunoblotting. (3) Results: miR-33a mimic treatment led to significantly downregulation of fatty acid synthase (FASN) in MCF-7 cells but not in MDA-MB-231 cells in the presence of estradiol-17β (E2) or Fulvestrant (FUL). In contrast to the miR-33a inhibitor effect, miR-33a mimic co-transfection with E2 or FUL led to diminished AMP-activated protein kinase α (AMPKα) activity in MCF-7 cells. E2 increases FASN levels in MDA-MB-231 cells regardless of miR-33a cellular levels. miR-33a inhibitor co-treatment suppressed E2-mediated AMPKα activity in MDA-MB-231 cells. (4) Conclusions: The cellular expression levels of miR-33a are critical to understanding differential responses which include cellular energy sensors such as AMPKα activation status in breast cancer cells.https://www.mdpi.com/2072-6694/13/21/5322estrogenbreast cancermiR-33aadipogenesisFASNfulvestrant |
| spellingShingle | Pelin Ozfiliz-Kilbas Ozlem Sonmez Pinar Obakan-Yerlikaya Ajda Coker-Gurkan Narcin Palavan-Ünsal Pinar Uysal-Onganer Elif Damla Arisan In Vitro Investigations of miR-33a Expression in Estrogen Receptor-Targeting Therapies in Breast Cancer Cells Cancers estrogen breast cancer miR-33a adipogenesis FASN fulvestrant |
| title | In Vitro Investigations of miR-33a Expression in Estrogen Receptor-Targeting Therapies in Breast Cancer Cells |
| title_full | In Vitro Investigations of miR-33a Expression in Estrogen Receptor-Targeting Therapies in Breast Cancer Cells |
| title_fullStr | In Vitro Investigations of miR-33a Expression in Estrogen Receptor-Targeting Therapies in Breast Cancer Cells |
| title_full_unstemmed | In Vitro Investigations of miR-33a Expression in Estrogen Receptor-Targeting Therapies in Breast Cancer Cells |
| title_short | In Vitro Investigations of miR-33a Expression in Estrogen Receptor-Targeting Therapies in Breast Cancer Cells |
| title_sort | in vitro investigations of mir 33a expression in estrogen receptor targeting therapies in breast cancer cells |
| topic | estrogen breast cancer miR-33a adipogenesis FASN fulvestrant |
| url | https://www.mdpi.com/2072-6694/13/21/5322 |
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