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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Autores principales:	Pelin Ozfiliz-Kilbas, Ozlem Sonmez, Pinar Obakan-Yerlikaya, Ajda Coker-Gurkan, Narcin Palavan-Ünsal, Pinar Uysal-Onganer, Elif Damla Arisan
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	estrogen breast cancer miR-33a adipogenesis FASN fulvestrant Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
Acceso en línea:	https://doaj.org/article/68b7df5e3f8c498a9e8a126c6d8ae068
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spelling	oai:doaj.org-article:68b7df5e3f8c498a9e8a126c6d8ae0682021-11-11T15:28:17ZIn Vitro Investigations of miR-33a Expression in Estrogen Receptor-Targeting Therapies in Breast Cancer Cells10.3390/cancers132153222072-6694https://doaj.org/article/68b7df5e3f8c498a9e8a126c6d8ae0682021-10-01T00:00:00Zhttps://www.mdpi.com/2072-6694/13/21/5322https://doaj.org/toc/2072-6694(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.Pelin Ozfiliz-KilbasOzlem SonmezPinar Obakan-YerlikayaAjda Coker-GurkanNarcin Palavan-ÜnsalPinar Uysal-OnganerElif Damla ArisanMDPI AGarticleestrogenbreast cancermiR-33aadipogenesisFASNfulvestrantNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282ENCancers, Vol 13, Iss 5322, p 5322 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	estrogen breast cancer miR-33a adipogenesis FASN fulvestrant Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
spellingShingle	estrogen breast cancer miR-33a adipogenesis FASN fulvestrant Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 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
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.
format	article
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
title	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_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_sort	in vitro investigations of mir-33a expression in estrogen receptor-targeting therapies in breast cancer cells
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/68b7df5e3f8c498a9e8a126c6d8ae068
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In Vitro Investigations of miR-33a Expression in Estrogen Receptor-Targeting Therapies in Breast Cancer Cells

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