Genome‐wide analysis reveals miR‐3184‐5p and miR‐181c‐3p as a critical regulator for adipocytes‐associated breast cancer
Obesity is considered as an independent risk factor for breast cancer (BCa) and plays a major role in the breast tumor microenvironment. The etiology and mechanisms by which obesity contributes to BCa development is not yet understood. Herein, we show that in vitro coculture of BCa cells with mature...
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description | Obesity is considered as an independent risk factor for breast cancer (BCa) and plays a major role in the breast tumor microenvironment. The etiology and mechanisms by which obesity contributes to BCa development is not yet understood. Herein, we show that in vitro coculture of BCa cells with mature adipocytes (MA‐BCa) increased proliferation, migration, and invasive phenotype of BCa cells. MA‐BCa coculture led to increased production of proinflammatory cytokines and chemokines. To identify microRNAs (miRNAs) in BCa cells that are modulated by the presence of adipocytes, we used small RNA sequencing analysis. Sequencing data revealed that 98 miRNAs were differentially expressed in MA‐BCa. Among them, miR‐3184‐5p and miR‐181c‐3p were found to be the most upregulated and downregulated miRNAs, and direct targets are FOXP4 and
PPARα, respectively. In vitro functional assays using a combination of miR‐3184‐5p inhibitor and miR‐181c‐3p mimic synergistically decreased adipocytes‐induced cell proliferation and invasive capacity of BCa cells. Gene Set Enrichment analysis indicated that transcription factors were highly enriched followed by protein kinases, oncogene, and protein regulators in MA‐BCa. GeneGo Metacore pathway analysis uncovered “NOTCH‐induced EMT pathway” was found to be the most abundant in MA‐BCa. Consistently, epithelial–mesenchymal transition‐associated markers were also increased in MA‐BCa. The disease enrichment analysis of the predict target genes revealed that diabetes mellitus was significantly affected disease in MA‐BCa. Taken together, our data suggest that miRNA‐based regulatory mechanism associated with deregulation of pathways and biological functions orchestrated by adipocytes‐secreted factors might drive the BCa progression and metastasis in obese patients.
Proposed model shows the modulation of microRNAs (miRNAs) in breast cancer (BCa) cells by the presence of mature adipocytes. |
doi_str_mv | 10.1002/jcp.28428 |
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PPARα, respectively. In vitro functional assays using a combination of miR‐3184‐5p inhibitor and miR‐181c‐3p mimic synergistically decreased adipocytes‐induced cell proliferation and invasive capacity of BCa cells. Gene Set Enrichment analysis indicated that transcription factors were highly enriched followed by protein kinases, oncogene, and protein regulators in MA‐BCa. GeneGo Metacore pathway analysis uncovered “NOTCH‐induced EMT pathway” was found to be the most abundant in MA‐BCa. Consistently, epithelial–mesenchymal transition‐associated markers were also increased in MA‐BCa. The disease enrichment analysis of the predict target genes revealed that diabetes mellitus was significantly affected disease in MA‐BCa. Taken together, our data suggest that miRNA‐based regulatory mechanism associated with deregulation of pathways and biological functions orchestrated by adipocytes‐secreted factors might drive the BCa progression and metastasis in obese patients.
Proposed model shows the modulation of microRNAs (miRNAs) in breast cancer (BCa) cells by the presence of mature adipocytes.</description><identifier>ISSN: 0021-9541</identifier><identifier>EISSN: 1097-4652</identifier><identifier>DOI: 10.1002/jcp.28428</identifier><identifier>PMID: 30847933</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>3T3 Cells ; Adenocarcinoma - genetics ; Adenocarcinoma - metabolism ; Adenocarcinoma - secondary ; Adipocytes ; Adipocytes - metabolism ; Adipocytes - pathology ; Animals ; Breast cancer ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cell Communication ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Chemokines ; Coculture Techniques ; Cytokines ; Cytokines - genetics ; Cytokines - metabolism ; Deregulation ; Diabetes mellitus ; Enrichment ; Epithelial-Mesenchymal Transition ; Etiology ; Female ; Forkhead Transcription Factors - genetics ; Forkhead Transcription Factors - metabolism ; Gene Expression Regulation, Neoplastic ; Gene sequencing ; Gene set enrichment analysis ; Genome-Wide Association Study ; Genomes ; Humans ; Inflammation ; Invasiveness ; Kinases ; Mesenchyme ; Metastases ; Mice ; microRNA ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Neoplasm Invasiveness ; Obesity ; Obesity - genetics ; Obesity - metabolism ; Obesity - pathology ; Phenotypes ; PPAR alpha - genetics ; PPAR alpha - metabolism ; Protein kinase ; Proteins ; Regulators ; Regulatory mechanisms (biology) ; Ribonucleic acid ; Risk analysis ; Risk factors ; RNA ; Signal Transduction ; small RNA sequencing ; Transcription factors ; Tumor Microenvironment</subject><ispartof>Journal of cellular physiology, 2019-10, Vol.234 (10), p.17959-17974</ispartof><rights>2019 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3538-444906c48250b97bf8a27cddec86b4a00e325a6fecf1d81f56d9fce3598bfda93</citedby><cites>FETCH-LOGICAL-c3538-444906c48250b97bf8a27cddec86b4a00e325a6fecf1d81f56d9fce3598bfda93</cites><orcidid>0000-0002-5351-9098</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcp.28428$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcp.28428$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30847933$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rajarajan, Dheeran</creatorcontrib><creatorcontrib>Selvarajan, Sweetha</creatorcontrib><creatorcontrib>Charan Raja, Mamilla R.</creatorcontrib><creatorcontrib>Kar Mahapatra, Santanu</creatorcontrib><creatorcontrib>Kasiappan, Ravi</creatorcontrib><title>Genome‐wide analysis reveals miR‐3184‐5p and miR‐181c‐3p as a critical regulator for adipocytes‐associated breast cancer</title><title>Journal of cellular physiology</title><addtitle>J Cell Physiol</addtitle><description>Obesity is considered as an independent risk factor for breast cancer (BCa) and plays a major role in the breast tumor microenvironment. The etiology and mechanisms by which obesity contributes to BCa development is not yet understood. Herein, we show that in vitro coculture of BCa cells with mature adipocytes (MA‐BCa) increased proliferation, migration, and invasive phenotype of BCa cells. MA‐BCa coculture led to increased production of proinflammatory cytokines and chemokines. To identify microRNAs (miRNAs) in BCa cells that are modulated by the presence of adipocytes, we used small RNA sequencing analysis. Sequencing data revealed that 98 miRNAs were differentially expressed in MA‐BCa. Among them, miR‐3184‐5p and miR‐181c‐3p were found to be the most upregulated and downregulated miRNAs, and direct targets are FOXP4 and
PPARα, respectively. In vitro functional assays using a combination of miR‐3184‐5p inhibitor and miR‐181c‐3p mimic synergistically decreased adipocytes‐induced cell proliferation and invasive capacity of BCa cells. Gene Set Enrichment analysis indicated that transcription factors were highly enriched followed by protein kinases, oncogene, and protein regulators in MA‐BCa. GeneGo Metacore pathway analysis uncovered “NOTCH‐induced EMT pathway” was found to be the most abundant in MA‐BCa. Consistently, epithelial–mesenchymal transition‐associated markers were also increased in MA‐BCa. The disease enrichment analysis of the predict target genes revealed that diabetes mellitus was significantly affected disease in MA‐BCa. Taken together, our data suggest that miRNA‐based regulatory mechanism associated with deregulation of pathways and biological functions orchestrated by adipocytes‐secreted factors might drive the BCa progression and metastasis in obese patients.
Proposed model shows the modulation of microRNAs (miRNAs) in breast cancer (BCa) cells by the presence of mature adipocytes.</description><subject>3T3 Cells</subject><subject>Adenocarcinoma - genetics</subject><subject>Adenocarcinoma - metabolism</subject><subject>Adenocarcinoma - secondary</subject><subject>Adipocytes</subject><subject>Adipocytes - metabolism</subject><subject>Adipocytes - pathology</subject><subject>Animals</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cell Communication</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Chemokines</subject><subject>Coculture Techniques</subject><subject>Cytokines</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Deregulation</subject><subject>Diabetes mellitus</subject><subject>Enrichment</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Etiology</subject><subject>Female</subject><subject>Forkhead Transcription Factors - genetics</subject><subject>Forkhead Transcription Factors - metabolism</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene sequencing</subject><subject>Gene set enrichment analysis</subject><subject>Genome-Wide Association Study</subject><subject>Genomes</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Invasiveness</subject><subject>Kinases</subject><subject>Mesenchyme</subject><subject>Metastases</subject><subject>Mice</subject><subject>microRNA</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Neoplasm Invasiveness</subject><subject>Obesity</subject><subject>Obesity - genetics</subject><subject>Obesity - metabolism</subject><subject>Obesity - pathology</subject><subject>Phenotypes</subject><subject>PPAR alpha - genetics</subject><subject>PPAR alpha - metabolism</subject><subject>Protein kinase</subject><subject>Proteins</subject><subject>Regulators</subject><subject>Regulatory mechanisms (biology)</subject><subject>Ribonucleic acid</subject><subject>Risk analysis</subject><subject>Risk factors</subject><subject>RNA</subject><subject>Signal Transduction</subject><subject>small RNA sequencing</subject><subject>Transcription factors</subject><subject>Tumor Microenvironment</subject><issn>0021-9541</issn><issn>1097-4652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc2KFDEUhYMoTju68AWkwI0uaia_VclSGh2VAUV0XdxKbiRNVVeZVDn0zoUP4DP6JN6xWxeCi3DDPV9O4BzGHgt-ITiXlzs_X0irpb3DNoK7ttaNkXfZhjRRO6PFGXtQyo5z7pxS99mZ4la3dN2w71e4n0b8-e3HTQpYwR6GQ0mlyvgVYSjVmD6QpoTVNMxMQDjthBX-VqJdqaDyOS3Jw0AvP68DLFOuIh0IaZ78YcFCLJQy-QQLhqrPCGWpPOw95ofsXqTP8NFpnrNPr15-3L6ur99dvdm-uK69MsrWWmvHG6-tNLx3bR8tyNaHgN42vQbOUUkDTUQfRbAimia46FEZZ_sYwKlz9uzoO-fpy4pl6cZUPA4D7HFaSyeFdYaC1JbQp_-gu2nNlA5RUjvlWgqTqOdHyueplIyxm3MaIR86wbvbajqqpvtdDbFPTo5rP2L4S_7pgoDLI3CTBjz836l7u31_tPwFfeyd1A</recordid><startdate>201910</startdate><enddate>201910</enddate><creator>Rajarajan, Dheeran</creator><creator>Selvarajan, Sweetha</creator><creator>Charan Raja, Mamilla R.</creator><creator>Kar Mahapatra, Santanu</creator><creator>Kasiappan, Ravi</creator><general>Wiley Subscription Services, Inc</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>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-5351-9098</orcidid></search><sort><creationdate>201910</creationdate><title>Genome‐wide analysis reveals miR‐3184‐5p and miR‐181c‐3p as a critical regulator for adipocytes‐associated breast cancer</title><author>Rajarajan, Dheeran ; Selvarajan, Sweetha ; Charan Raja, Mamilla R. ; Kar Mahapatra, Santanu ; Kasiappan, Ravi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3538-444906c48250b97bf8a27cddec86b4a00e325a6fecf1d81f56d9fce3598bfda93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>3T3 Cells</topic><topic>Adenocarcinoma - genetics</topic><topic>Adenocarcinoma - metabolism</topic><topic>Adenocarcinoma - secondary</topic><topic>Adipocytes</topic><topic>Adipocytes - metabolism</topic><topic>Adipocytes - pathology</topic><topic>Animals</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cell Communication</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Chemokines</topic><topic>Coculture Techniques</topic><topic>Cytokines</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Deregulation</topic><topic>Diabetes mellitus</topic><topic>Enrichment</topic><topic>Epithelial-Mesenchymal Transition</topic><topic>Etiology</topic><topic>Female</topic><topic>Forkhead Transcription Factors - genetics</topic><topic>Forkhead Transcription Factors - metabolism</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene sequencing</topic><topic>Gene set enrichment analysis</topic><topic>Genome-Wide Association Study</topic><topic>Genomes</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Invasiveness</topic><topic>Kinases</topic><topic>Mesenchyme</topic><topic>Metastases</topic><topic>Mice</topic><topic>microRNA</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>Neoplasm Invasiveness</topic><topic>Obesity</topic><topic>Obesity - genetics</topic><topic>Obesity - metabolism</topic><topic>Obesity - pathology</topic><topic>Phenotypes</topic><topic>PPAR alpha - genetics</topic><topic>PPAR alpha - metabolism</topic><topic>Protein kinase</topic><topic>Proteins</topic><topic>Regulators</topic><topic>Regulatory mechanisms (biology)</topic><topic>Ribonucleic acid</topic><topic>Risk analysis</topic><topic>Risk factors</topic><topic>RNA</topic><topic>Signal Transduction</topic><topic>small RNA sequencing</topic><topic>Transcription factors</topic><topic>Tumor Microenvironment</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rajarajan, Dheeran</creatorcontrib><creatorcontrib>Selvarajan, Sweetha</creatorcontrib><creatorcontrib>Charan Raja, Mamilla R.</creatorcontrib><creatorcontrib>Kar Mahapatra, Santanu</creatorcontrib><creatorcontrib>Kasiappan, Ravi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rajarajan, Dheeran</au><au>Selvarajan, Sweetha</au><au>Charan Raja, Mamilla R.</au><au>Kar Mahapatra, Santanu</au><au>Kasiappan, Ravi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genome‐wide analysis reveals miR‐3184‐5p and miR‐181c‐3p as a critical regulator for adipocytes‐associated breast cancer</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J Cell Physiol</addtitle><date>2019-10</date><risdate>2019</risdate><volume>234</volume><issue>10</issue><spage>17959</spage><epage>17974</epage><pages>17959-17974</pages><issn>0021-9541</issn><eissn>1097-4652</eissn><abstract>Obesity is considered as an independent risk factor for breast cancer (BCa) and plays a major role in the breast tumor microenvironment. The etiology and mechanisms by which obesity contributes to BCa development is not yet understood. Herein, we show that in vitro coculture of BCa cells with mature adipocytes (MA‐BCa) increased proliferation, migration, and invasive phenotype of BCa cells. MA‐BCa coculture led to increased production of proinflammatory cytokines and chemokines. To identify microRNAs (miRNAs) in BCa cells that are modulated by the presence of adipocytes, we used small RNA sequencing analysis. Sequencing data revealed that 98 miRNAs were differentially expressed in MA‐BCa. Among them, miR‐3184‐5p and miR‐181c‐3p were found to be the most upregulated and downregulated miRNAs, and direct targets are FOXP4 and
PPARα, respectively. In vitro functional assays using a combination of miR‐3184‐5p inhibitor and miR‐181c‐3p mimic synergistically decreased adipocytes‐induced cell proliferation and invasive capacity of BCa cells. Gene Set Enrichment analysis indicated that transcription factors were highly enriched followed by protein kinases, oncogene, and protein regulators in MA‐BCa. GeneGo Metacore pathway analysis uncovered “NOTCH‐induced EMT pathway” was found to be the most abundant in MA‐BCa. Consistently, epithelial–mesenchymal transition‐associated markers were also increased in MA‐BCa. The disease enrichment analysis of the predict target genes revealed that diabetes mellitus was significantly affected disease in MA‐BCa. Taken together, our data suggest that miRNA‐based regulatory mechanism associated with deregulation of pathways and biological functions orchestrated by adipocytes‐secreted factors might drive the BCa progression and metastasis in obese patients.
Proposed model shows the modulation of microRNAs (miRNAs) in breast cancer (BCa) cells by the presence of mature adipocytes.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>30847933</pmid><doi>10.1002/jcp.28428</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0002-5351-9098</orcidid></addata></record> |
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subjects | 3T3 Cells Adenocarcinoma - genetics Adenocarcinoma - metabolism Adenocarcinoma - secondary Adipocytes Adipocytes - metabolism Adipocytes - pathology Animals Breast cancer Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Cell Communication Cell Line, Tumor Cell Movement Cell Proliferation Chemokines Coculture Techniques Cytokines Cytokines - genetics Cytokines - metabolism Deregulation Diabetes mellitus Enrichment Epithelial-Mesenchymal Transition Etiology Female Forkhead Transcription Factors - genetics Forkhead Transcription Factors - metabolism Gene Expression Regulation, Neoplastic Gene sequencing Gene set enrichment analysis Genome-Wide Association Study Genomes Humans Inflammation Invasiveness Kinases Mesenchyme Metastases Mice microRNA MicroRNAs - genetics MicroRNAs - metabolism miRNA Neoplasm Invasiveness Obesity Obesity - genetics Obesity - metabolism Obesity - pathology Phenotypes PPAR alpha - genetics PPAR alpha - metabolism Protein kinase Proteins Regulators Regulatory mechanisms (biology) Ribonucleic acid Risk analysis Risk factors RNA Signal Transduction small RNA sequencing Transcription factors Tumor Microenvironment |
title | Genome‐wide analysis reveals miR‐3184‐5p and miR‐181c‐3p as a critical regulator for adipocytes‐associated breast cancer |
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