CEBP-β and PLK1 as Potential Mediators of the Breast Cancer/Obesity Crosstalk: In Vitro and In Silico Analyses
Over the last two decades, obesity has reached pandemic proportions in several countries, and expanding evidence is showing its contribution to several types of malignancies, including breast cancer (BC). The conditioned medium (CM) from mature adipocytes contains a complex of secretes that may mimi...
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| Veröffentlicht in: | Nutrients 2023-06, Vol.15 (13), p.2839 |
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| creator | Accattatis, Felice Maria Caruso, Amanda Carleo, Alfonso Del Console, Piercarlo Gelsomino, Luca Bonofiglio, Daniela Giordano, Cinzia Barone, Ines Andò, Sebastiano Bianchi, Laura Catalano, Stefania |
| description | Over the last two decades, obesity has reached pandemic proportions in several countries, and expanding evidence is showing its contribution to several types of malignancies, including breast cancer (BC). The conditioned medium (CM) from mature adipocytes contains a complex of secretes that may mimic the obesity condition in studies on BC cell lines conducted in vitro. Here, we report a transcriptomic analysis on MCF-7 BC cells exposed to adipocyte-derived CM and focus on the predictive functional relevance that CM-affected pathways/processes and related biomarkers (BMs) may have in BC response to obesity. CM was demonstrated to increase cell proliferation, motility and invasion as well as broadly alter the transcript profiles of MCF-7 cells by significantly modulating 364 genes. Bioinformatic functional analyses unraveled the presence of five highly relevant central hubs in the direct interaction networks (DIN), and Kaplan-Meier analysis sorted the CCAAT/enhancer binding protein beta (CEBP-β) and serine/threonine-protein kinase PLK1 (PLK1) as clinically significant biomarkers in BC. Indeed, CEBP-β and PLK1 negatively correlated with BC overall survival and were up-regulated by adipocyte-derived CM. In addition to their known involvement in cell proliferation and tumor progression, our work suggests them as a possible "deus ex machina" in BC response to fat tissue humoral products in obese women. |
| doi_str_mv | 10.3390/nu15132839 |
| format | Article |
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The conditioned medium (CM) from mature adipocytes contains a complex of secretes that may mimic the obesity condition in studies on BC cell lines conducted in vitro. Here, we report a transcriptomic analysis on MCF-7 BC cells exposed to adipocyte-derived CM and focus on the predictive functional relevance that CM-affected pathways/processes and related biomarkers (BMs) may have in BC response to obesity. CM was demonstrated to increase cell proliferation, motility and invasion as well as broadly alter the transcript profiles of MCF-7 cells by significantly modulating 364 genes. Bioinformatic functional analyses unraveled the presence of five highly relevant central hubs in the direct interaction networks (DIN), and Kaplan-Meier analysis sorted the CCAAT/enhancer binding protein beta (CEBP-β) and serine/threonine-protein kinase PLK1 (PLK1) as clinically significant biomarkers in BC. Indeed, CEBP-β and PLK1 negatively correlated with BC overall survival and were up-regulated by adipocyte-derived CM. In addition to their known involvement in cell proliferation and tumor progression, our work suggests them as a possible "deus ex machina" in BC response to fat tissue humoral products in obese women.</description><identifier>ISSN: 2072-6643</identifier><identifier>EISSN: 2072-6643</identifier><identifier>DOI: 10.3390/nu15132839</identifier><identifier>PMID: 37447165</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Adipocytes ; Adipocytes - metabolism ; Adipose Tissue - metabolism ; Antibodies ; Biomarkers ; Body mass index ; Breast cancer ; Breast Neoplasms - metabolism ; Cancer therapies ; CCAAT/enhancer-binding protein ; Cell Line, Tumor ; Cell Proliferation ; Cells ; Female ; Gene expression ; Humans ; Insulin ; Integrated software ; Kinases ; Lipids ; Malignancy ; MCF-7 Cells ; Medical prognosis ; Medical research ; Obesity ; Obesity - metabolism ; Ontology ; Overweight ; Physiology ; Polo-like kinase 1 ; Protein binding ; Protein kinases ; Proteins ; Transcriptomics ; Type 2 diabetes ; Womens health</subject><ispartof>Nutrients, 2023-06, Vol.15 (13), p.2839</ispartof><rights>COPYRIGHT 2023 MDPI AG</rights><rights>2023 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><rights>2023 by the authors. 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-74773de591cc111ea1b67d3a4b16fe1532015e6bdf72410b8df1d15141b7bb3a3</citedby><cites>FETCH-LOGICAL-c474t-74773de591cc111ea1b67d3a4b16fe1532015e6bdf72410b8df1d15141b7bb3a3</cites><orcidid>0000-0001-9219-1227 ; 0000-0002-4142-0496 ; 0000-0002-9769-1615</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10343266/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10343266/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37447165$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Accattatis, Felice Maria</creatorcontrib><creatorcontrib>Caruso, Amanda</creatorcontrib><creatorcontrib>Carleo, Alfonso</creatorcontrib><creatorcontrib>Del Console, Piercarlo</creatorcontrib><creatorcontrib>Gelsomino, Luca</creatorcontrib><creatorcontrib>Bonofiglio, Daniela</creatorcontrib><creatorcontrib>Giordano, Cinzia</creatorcontrib><creatorcontrib>Barone, Ines</creatorcontrib><creatorcontrib>Andò, Sebastiano</creatorcontrib><creatorcontrib>Bianchi, Laura</creatorcontrib><creatorcontrib>Catalano, Stefania</creatorcontrib><title>CEBP-β and PLK1 as Potential Mediators of the Breast Cancer/Obesity Crosstalk: In Vitro and In Silico Analyses</title><title>Nutrients</title><addtitle>Nutrients</addtitle><description>Over the last two decades, obesity has reached pandemic proportions in several countries, and expanding evidence is showing its contribution to several types of malignancies, including breast cancer (BC). The conditioned medium (CM) from mature adipocytes contains a complex of secretes that may mimic the obesity condition in studies on BC cell lines conducted in vitro. Here, we report a transcriptomic analysis on MCF-7 BC cells exposed to adipocyte-derived CM and focus on the predictive functional relevance that CM-affected pathways/processes and related biomarkers (BMs) may have in BC response to obesity. CM was demonstrated to increase cell proliferation, motility and invasion as well as broadly alter the transcript profiles of MCF-7 cells by significantly modulating 364 genes. Bioinformatic functional analyses unraveled the presence of five highly relevant central hubs in the direct interaction networks (DIN), and Kaplan-Meier analysis sorted the CCAAT/enhancer binding protein beta (CEBP-β) and serine/threonine-protein kinase PLK1 (PLK1) as clinically significant biomarkers in BC. 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In addition to their known involvement in cell proliferation and tumor progression, our work suggests them as a possible "deus ex machina" in BC response to fat tissue humoral products in obese women.</description><subject>Adipocytes</subject><subject>Adipocytes - metabolism</subject><subject>Adipose Tissue - metabolism</subject><subject>Antibodies</subject><subject>Biomarkers</subject><subject>Body mass index</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - metabolism</subject><subject>Cancer therapies</subject><subject>CCAAT/enhancer-binding protein</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Cells</subject><subject>Female</subject><subject>Gene expression</subject><subject>Humans</subject><subject>Insulin</subject><subject>Integrated software</subject><subject>Kinases</subject><subject>Lipids</subject><subject>Malignancy</subject><subject>MCF-7 Cells</subject><subject>Medical prognosis</subject><subject>Medical research</subject><subject>Obesity</subject><subject>Obesity - metabolism</subject><subject>Ontology</subject><subject>Overweight</subject><subject>Physiology</subject><subject>Polo-like kinase 1</subject><subject>Protein binding</subject><subject>Protein kinases</subject><subject>Proteins</subject><subject>Transcriptomics</subject><subject>Type 2 diabetes</subject><subject>Womens health</subject><issn>2072-6643</issn><issn>2072-6643</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkt1uFCEUx4nR2Kb2xgcwJN4Yk2n5Gpj1xmwntTau6SZ-3BJmONNSZ6EC02Rfqw_iM5Vtaz-McMEBfudPzp-D0GtK9jifkX0_0Zpy1vDZM7TNiGKVlII_fxRvod2UzslmKKIkf4m2uBJCUVlvo9AeHiyrP1fYeIuXiy8Um4SXIYPPzoz4K1hncogJhwHnM8AHEUzKuDW-h7h_0kFyeY3bGFLKZvz1AR97_NPlGG4Ey-abG10f8NybcZ0gvUIvBjMm2L1bd9CPT4ff28_V4uTouJ0vql4okSsllOIW6hnte0opGNpJZbkRHZUD0JozQmuQnR0UE5R0jR2oLUYI2qmu44bvoI-3uhdTtwLbl3qiGfVFdCsT1zoYp5_eeHemT8OlpoQLzqQsCu_uFGL4PUHKeuVSD-NoPIQp6WJ5w0TdqFlB3_6DnocplopvKCkI45w8UKdmBO38EMrD_UZUz1XdCEZkrQq19x-qTAurYqSHwZXzJwnvbxP6zSdEGO6LpERvWkQ_tEiB3zy25R792xD8Gsuvs9w</recordid><startdate>20230622</startdate><enddate>20230622</enddate><creator>Accattatis, Felice Maria</creator><creator>Caruso, Amanda</creator><creator>Carleo, Alfonso</creator><creator>Del Console, Piercarlo</creator><creator>Gelsomino, Luca</creator><creator>Bonofiglio, Daniela</creator><creator>Giordano, Cinzia</creator><creator>Barone, Ines</creator><creator>Andò, Sebastiano</creator><creator>Bianchi, Laura</creator><creator>Catalano, Stefania</creator><general>MDPI AG</general><general>MDPI</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>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</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>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-9219-1227</orcidid><orcidid>https://orcid.org/0000-0002-4142-0496</orcidid><orcidid>https://orcid.org/0000-0002-9769-1615</orcidid></search><sort><creationdate>20230622</creationdate><title>CEBP-β and PLK1 as Potential Mediators of the Breast Cancer/Obesity Crosstalk: In Vitro and In Silico Analyses</title><author>Accattatis, Felice Maria ; 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The conditioned medium (CM) from mature adipocytes contains a complex of secretes that may mimic the obesity condition in studies on BC cell lines conducted in vitro. Here, we report a transcriptomic analysis on MCF-7 BC cells exposed to adipocyte-derived CM and focus on the predictive functional relevance that CM-affected pathways/processes and related biomarkers (BMs) may have in BC response to obesity. CM was demonstrated to increase cell proliferation, motility and invasion as well as broadly alter the transcript profiles of MCF-7 cells by significantly modulating 364 genes. Bioinformatic functional analyses unraveled the presence of five highly relevant central hubs in the direct interaction networks (DIN), and Kaplan-Meier analysis sorted the CCAAT/enhancer binding protein beta (CEBP-β) and serine/threonine-protein kinase PLK1 (PLK1) as clinically significant biomarkers in BC. Indeed, CEBP-β and PLK1 negatively correlated with BC overall survival and were up-regulated by adipocyte-derived CM. In addition to their known involvement in cell proliferation and tumor progression, our work suggests them as a possible "deus ex machina" in BC response to fat tissue humoral products in obese women.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>37447165</pmid><doi>10.3390/nu15132839</doi><orcidid>https://orcid.org/0000-0001-9219-1227</orcidid><orcidid>https://orcid.org/0000-0002-4142-0496</orcidid><orcidid>https://orcid.org/0000-0002-9769-1615</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adipocytes Adipocytes - metabolism Adipose Tissue - metabolism Antibodies Biomarkers Body mass index Breast cancer Breast Neoplasms - metabolism Cancer therapies CCAAT/enhancer-binding protein Cell Line, Tumor Cell Proliferation Cells Female Gene expression Humans Insulin Integrated software Kinases Lipids Malignancy MCF-7 Cells Medical prognosis Medical research Obesity Obesity - metabolism Ontology Overweight Physiology Polo-like kinase 1 Protein binding Protein kinases Proteins Transcriptomics Type 2 diabetes Womens health |
| title | CEBP-β and PLK1 as Potential Mediators of the Breast Cancer/Obesity Crosstalk: In Vitro and In Silico Analyses |
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