Loss of Hormone Receptor Expression after Exposure to Fluid Shear Stress in Breast Cancer Cell Lines
Following metastatic spread, many hormone receptor positive (HR ) patients develop a more aggressive phenotype with an observed loss of the HRs estrogen receptor (ER) and progesterone receptor (PR). During metastasis, breast cancer cells are exposed to high magnitudes of fluid shear stress (FSS). Un...
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| Veröffentlicht in: | International journal of molecular sciences 2024-06, Vol.25 (13), p.7119 |
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| creator | Cuccia, Jonathan Ortega Quesada, Braulio Andrés Littlefield, Ethan P Ham, Alejandra M Burow, Matthew E Melvin, Adam T Martin, Elizabeth C |
| description | Following metastatic spread, many hormone receptor positive (HR
) patients develop a more aggressive phenotype with an observed loss of the HRs estrogen receptor (ER) and progesterone receptor (PR). During metastasis, breast cancer cells are exposed to high magnitudes of fluid shear stress (FSS). Unfortunately, the role for FSS on the regulation of HR expression and function during metastasis is not fully understood. This study was designed to elucidate the impact of FSS on HR
breast cancer. Utilizing a microfluidic platform capable of exposing breast cancer cells to FSS that mimics in situ conditions, we demonstrate the impact of FSS exposure on representative HR
breast cancer cell lines through protein and gene expression analysis. Proteomics results demonstrated that 540 total proteins and 1473 phospho-proteins significantly changed due to FSS exposure and pathways of interest included early and late estrogen response. The impact of FSS on response to 17β-estradiol (E2) was next evaluated and gene expression analysis revealed repression of ER and E2-mediated genes (
and
) following exposure to FSS. Western blot demonstrated enhanced phosphorylation of mTOR following exposure to FSS. Taken together, these studies provide initial insight into the effects of FSS on HR signaling in metastatic breast cancer. |
| doi_str_mv | 10.3390/ijms25137119 |
| format | Article |
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) patients develop a more aggressive phenotype with an observed loss of the HRs estrogen receptor (ER) and progesterone receptor (PR). During metastasis, breast cancer cells are exposed to high magnitudes of fluid shear stress (FSS). Unfortunately, the role for FSS on the regulation of HR expression and function during metastasis is not fully understood. This study was designed to elucidate the impact of FSS on HR
breast cancer. Utilizing a microfluidic platform capable of exposing breast cancer cells to FSS that mimics in situ conditions, we demonstrate the impact of FSS exposure on representative HR
breast cancer cell lines through protein and gene expression analysis. Proteomics results demonstrated that 540 total proteins and 1473 phospho-proteins significantly changed due to FSS exposure and pathways of interest included early and late estrogen response. The impact of FSS on response to 17β-estradiol (E2) was next evaluated and gene expression analysis revealed repression of ER and E2-mediated genes (
and
) following exposure to FSS. Western blot demonstrated enhanced phosphorylation of mTOR following exposure to FSS. Taken together, these studies provide initial insight into the effects of FSS on HR signaling in metastatic breast cancer.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms25137119</identifier><identifier>PMID: 39000231</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Breast cancer ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cell death ; Cell Line, Tumor ; Chemokine CXCL12 - genetics ; Chemokine CXCL12 - metabolism ; Estradiol - pharmacology ; Estrogens ; Female ; Gene expression ; Gene Expression Regulation, Neoplastic ; Growth factors ; Humans ; MCF-7 Cells ; Metastasis ; Phosphorylation ; Proteins ; Proteomics ; Proteomics - methods ; Receptors, Estrogen - genetics ; Receptors, Estrogen - metabolism ; Receptors, Progesterone - genetics ; Receptors, Progesterone - metabolism ; Shear stress ; Signal Transduction ; Stress, Mechanical ; TOR Serine-Threonine Kinases - metabolism ; Trends ; Tumors</subject><ispartof>International journal of molecular sciences, 2024-06, Vol.25 (13), p.7119</ispartof><rights>2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c244t-d90cb8c69b95ac4320094050e33a4cf8bcd127071bf1a21c3eaa71354727f5813</cites><orcidid>0000-0002-0642-6630 ; 0000-0003-0484-5871</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39000231$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cuccia, Jonathan</creatorcontrib><creatorcontrib>Ortega Quesada, Braulio Andrés</creatorcontrib><creatorcontrib>Littlefield, Ethan P</creatorcontrib><creatorcontrib>Ham, Alejandra M</creatorcontrib><creatorcontrib>Burow, Matthew E</creatorcontrib><creatorcontrib>Melvin, Adam T</creatorcontrib><creatorcontrib>Martin, Elizabeth C</creatorcontrib><title>Loss of Hormone Receptor Expression after Exposure to Fluid Shear Stress in Breast Cancer Cell Lines</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Following metastatic spread, many hormone receptor positive (HR
) patients develop a more aggressive phenotype with an observed loss of the HRs estrogen receptor (ER) and progesterone receptor (PR). During metastasis, breast cancer cells are exposed to high magnitudes of fluid shear stress (FSS). Unfortunately, the role for FSS on the regulation of HR expression and function during metastasis is not fully understood. This study was designed to elucidate the impact of FSS on HR
breast cancer. Utilizing a microfluidic platform capable of exposing breast cancer cells to FSS that mimics in situ conditions, we demonstrate the impact of FSS exposure on representative HR
breast cancer cell lines through protein and gene expression analysis. Proteomics results demonstrated that 540 total proteins and 1473 phospho-proteins significantly changed due to FSS exposure and pathways of interest included early and late estrogen response. The impact of FSS on response to 17β-estradiol (E2) was next evaluated and gene expression analysis revealed repression of ER and E2-mediated genes (
and
) following exposure to FSS. Western blot demonstrated enhanced phosphorylation of mTOR following exposure to FSS. Taken together, these studies provide initial insight into the effects of FSS on HR signaling in metastatic breast cancer.</description><subject>Breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cell death</subject><subject>Cell Line, Tumor</subject><subject>Chemokine CXCL12 - genetics</subject><subject>Chemokine CXCL12 - metabolism</subject><subject>Estradiol - pharmacology</subject><subject>Estrogens</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Growth factors</subject><subject>Humans</subject><subject>MCF-7 Cells</subject><subject>Metastasis</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Proteomics</subject><subject>Proteomics - methods</subject><subject>Receptors, Estrogen - genetics</subject><subject>Receptors, Estrogen - metabolism</subject><subject>Receptors, Progesterone - genetics</subject><subject>Receptors, Progesterone - metabolism</subject><subject>Shear stress</subject><subject>Signal Transduction</subject><subject>Stress, Mechanical</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><subject>Trends</subject><subject>Tumors</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkM1LwzAYh4Mobk5vniXgxYPVfLRLc9SyOaEgOD2XNH2LGW1Tkxb0v7fdpgxP7wfP--PlQeiSkjvOJbk3m9qziHJBqTxCUxoyFhAyF8cH_QSdeb8hhHEWyVM0Ge7GgU5RkVrvsS3xyrraNoBfQUPbWYcXX60D741tsCo72C6s7x3gzuJl1ZsCrz9AObzuRg6bBj86UL7DiWr0wCdQVTg1DfhzdFKqysPFvs7Q-3LxlqyC9OXpOXlIA83CsAsKSXQe67nMZaR0yBkhMiQRAc5VqMs41wVlggial1QxqjkoJSiPQsFEGcWUz9DNLrd19rMH32W18Xp4QzVge59xImQ8p5TwAb3-h25s75rhuy3FGePRGHi7o7QbNDkos9aZWrnvjJJstJ8d2h_wq31on9dQ_MG_uvkPmxx-gQ</recordid><startdate>20240628</startdate><enddate>20240628</enddate><creator>Cuccia, Jonathan</creator><creator>Ortega Quesada, Braulio Andrés</creator><creator>Littlefield, Ethan P</creator><creator>Ham, Alejandra M</creator><creator>Burow, Matthew E</creator><creator>Melvin, Adam T</creator><creator>Martin, Elizabeth C</creator><general>MDPI AG</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-0642-6630</orcidid><orcidid>https://orcid.org/0000-0003-0484-5871</orcidid></search><sort><creationdate>20240628</creationdate><title>Loss of Hormone Receptor Expression after Exposure to Fluid Shear Stress in Breast Cancer Cell Lines</title><author>Cuccia, Jonathan ; Ortega Quesada, Braulio Andrés ; Littlefield, Ethan P ; Ham, Alejandra M ; Burow, Matthew E ; Melvin, Adam T ; Martin, Elizabeth C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c244t-d90cb8c69b95ac4320094050e33a4cf8bcd127071bf1a21c3eaa71354727f5813</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Breast cancer</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cell death</topic><topic>Cell Line, Tumor</topic><topic>Chemokine CXCL12 - genetics</topic><topic>Chemokine CXCL12 - metabolism</topic><topic>Estradiol - pharmacology</topic><topic>Estrogens</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Growth factors</topic><topic>Humans</topic><topic>MCF-7 Cells</topic><topic>Metastasis</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>Proteomics</topic><topic>Proteomics - methods</topic><topic>Receptors, Estrogen - genetics</topic><topic>Receptors, Estrogen - metabolism</topic><topic>Receptors, Progesterone - genetics</topic><topic>Receptors, Progesterone - metabolism</topic><topic>Shear stress</topic><topic>Signal Transduction</topic><topic>Stress, Mechanical</topic><topic>TOR Serine-Threonine Kinases - metabolism</topic><topic>Trends</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cuccia, Jonathan</creatorcontrib><creatorcontrib>Ortega Quesada, Braulio Andrés</creatorcontrib><creatorcontrib>Littlefield, Ethan P</creatorcontrib><creatorcontrib>Ham, Alejandra M</creatorcontrib><creatorcontrib>Burow, Matthew E</creatorcontrib><creatorcontrib>Melvin, Adam T</creatorcontrib><creatorcontrib>Martin, Elizabeth C</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cuccia, Jonathan</au><au>Ortega Quesada, Braulio Andrés</au><au>Littlefield, Ethan P</au><au>Ham, Alejandra M</au><au>Burow, Matthew E</au><au>Melvin, Adam T</au><au>Martin, Elizabeth C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Loss of Hormone Receptor Expression after Exposure to Fluid Shear Stress in Breast Cancer Cell Lines</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2024-06-28</date><risdate>2024</risdate><volume>25</volume><issue>13</issue><spage>7119</spage><pages>7119-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Following metastatic spread, many hormone receptor positive (HR
) patients develop a more aggressive phenotype with an observed loss of the HRs estrogen receptor (ER) and progesterone receptor (PR). During metastasis, breast cancer cells are exposed to high magnitudes of fluid shear stress (FSS). Unfortunately, the role for FSS on the regulation of HR expression and function during metastasis is not fully understood. This study was designed to elucidate the impact of FSS on HR
breast cancer. Utilizing a microfluidic platform capable of exposing breast cancer cells to FSS that mimics in situ conditions, we demonstrate the impact of FSS exposure on representative HR
breast cancer cell lines through protein and gene expression analysis. Proteomics results demonstrated that 540 total proteins and 1473 phospho-proteins significantly changed due to FSS exposure and pathways of interest included early and late estrogen response. The impact of FSS on response to 17β-estradiol (E2) was next evaluated and gene expression analysis revealed repression of ER and E2-mediated genes (
and
) following exposure to FSS. Western blot demonstrated enhanced phosphorylation of mTOR following exposure to FSS. Taken together, these studies provide initial insight into the effects of FSS on HR signaling in metastatic breast cancer.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>39000231</pmid><doi>10.3390/ijms25137119</doi><orcidid>https://orcid.org/0000-0002-0642-6630</orcidid><orcidid>https://orcid.org/0000-0003-0484-5871</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; MDPI - Multidisciplinary Digital Publishing Institute; PubMed Central |
| subjects | Breast cancer Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Cell death Cell Line, Tumor Chemokine CXCL12 - genetics Chemokine CXCL12 - metabolism Estradiol - pharmacology Estrogens Female Gene expression Gene Expression Regulation, Neoplastic Growth factors Humans MCF-7 Cells Metastasis Phosphorylation Proteins Proteomics Proteomics - methods Receptors, Estrogen - genetics Receptors, Estrogen - metabolism Receptors, Progesterone - genetics Receptors, Progesterone - metabolism Shear stress Signal Transduction Stress, Mechanical TOR Serine-Threonine Kinases - metabolism Trends Tumors |
| title | Loss of Hormone Receptor Expression after Exposure to Fluid Shear Stress in Breast Cancer Cell Lines |
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