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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Veröffentlicht in:Journal of cellular physiology 2019-10, Vol.234 (10), p.17959-17974
Hauptverfasser: Rajarajan, Dheeran, Selvarajan, Sweetha, Charan Raja, Mamilla R., Kar Mahapatra, Santanu, Kasiappan, Ravi
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container_end_page 17974
container_issue 10
container_start_page 17959
container_title Journal of cellular physiology
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creator Rajarajan, Dheeran
Selvarajan, Sweetha
Charan Raja, Mamilla R.
Kar Mahapatra, Santanu
Kasiappan, Ravi
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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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><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. 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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 &amp; 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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. 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source MEDLINE; Wiley Online Library Journals Frontfile Complete
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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