Small interfering RNA against transcription factor STAT6 leads to increased cholesterol synthesis in lung cancer cell lines
STAT6 transcription factor has become a potential molecule for therapeutic intervention because it regulates broad range of cellular processes in a large variety of cell types. Although some target genes and interacting partners of STAT6 have been identified, its exact mechanism of action needs to b...
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| description | STAT6 transcription factor has become a potential molecule for therapeutic intervention because it regulates broad range of cellular processes in a large variety of cell types. Although some target genes and interacting partners of STAT6 have been identified, its exact mechanism of action needs to be elucidated. In this study, we sought to further characterize the molecular interactions, networks, and functions of STAT6 by profiling the mRNA expression of STAT6 silenced human lung cells (NCI-H460) using microarrays. Our analysis revealed 273 differentially expressed genes after STAT6 silencing. Analysis of the gene expression data with Ingenuity Pathway Analysis (IPA) software revealed Gene expression, Cell death, Lipid metabolism as the functions associated with highest rated network. Cholesterol biosynthesis was among the most enriched pathways in IPA as well as in PANTHER analysis. These results have been validated by real-time PCR and cholesterol assay using scrambled siRNA as a negative control. Similar findings were also observed with human type II pulmonary alveolar epithelial cells, A549. In the present study we have, for the first time, shown the inverse relationship of STAT6 with the cholesterol biosynthesis in lung cancer cells. The present findings are potentially significant to advance the understanding and design of therapeutics for the pathological conditions where both STAT6 and cholesterol biosynthesis are implicated viz. asthma, atherosclerosis etc. |
| doi_str_mv | 10.1371/journal.pone.0028509 |
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In the present study we have, for the first time, shown the inverse relationship of STAT6 with the cholesterol biosynthesis in lung cancer cells. The present findings are potentially significant to advance the understanding and design of therapeutics for the pathological conditions where both STAT6 and cholesterol biosynthesis are implicated viz. asthma, atherosclerosis etc.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0028509</identifier><identifier>PMID: 22162773</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Allergies ; Alveoli ; Analysis ; Annexin A5 - pharmacology ; Apoptosis ; Arteriosclerosis ; Asthma ; Atherosclerosis ; Biology ; Biosynthesis ; Cancer ; Carcinoma - metabolism ; Cell death ; Cell Line, Tumor ; Cholesterol ; Cholesterol - chemistry ; Cholesterol - metabolism ; Computational Biology - methods ; Cytokines ; Data processing ; Deoxyribonucleic acid ; DNA ; DNA microarrays ; Down-Regulation ; Epithelial cells ; Fluorides ; Forkhead Transcription Factors - metabolism ; Gene expression ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gene Silencing ; Genes ; Genomics ; Health aspects ; Hepatitis ; Humans ; Inflammation ; Kinases ; Lipid metabolism ; Lipids ; Lung cancer ; Lung diseases ; Lung Neoplasms - metabolism ; Lymphoma ; Medicine ; Metabolism ; Molecular interactions ; Oligonucleotide Array Sequence Analysis ; Promoter Regions, Genetic ; Proteins ; Ribonucleic acid ; RNA ; RNA, Small Interfering - metabolism ; Rodents ; siRNA ; Stat6 protein ; STAT6 Transcription Factor - metabolism ; Transcription factors ; Transcription, Genetic ; Tumor cell lines</subject><ispartof>PloS one, 2011-12, Vol.6 (12), p.e28509-e28509</ispartof><rights>COPYRIGHT 2011 Public Library of Science</rights><rights>2011 Dubey et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Dubey et al. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c691t-c74aa8efdc3a4e6bf8c379f0e2ae7a5dec931985de31489a1c2a22c876bff0ee3</citedby><cites>FETCH-LOGICAL-c691t-c74aa8efdc3a4e6bf8c379f0e2ae7a5dec931985de31489a1c2a22c876bff0ee3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3230611/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3230611/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22162773$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dubey, Richa</creatorcontrib><creatorcontrib>Chhabra, Ravindresh</creatorcontrib><creatorcontrib>Saini, Neeru</creatorcontrib><title>Small interfering RNA against transcription factor STAT6 leads to increased cholesterol synthesis in lung cancer cell lines</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>STAT6 transcription factor has become a potential molecule for therapeutic intervention because it regulates broad range of cellular processes in a large variety of cell types. Although some target genes and interacting partners of STAT6 have been identified, its exact mechanism of action needs to be elucidated. In this study, we sought to further characterize the molecular interactions, networks, and functions of STAT6 by profiling the mRNA expression of STAT6 silenced human lung cells (NCI-H460) using microarrays. Our analysis revealed 273 differentially expressed genes after STAT6 silencing. Analysis of the gene expression data with Ingenuity Pathway Analysis (IPA) software revealed Gene expression, Cell death, Lipid metabolism as the functions associated with highest rated network. Cholesterol biosynthesis was among the most enriched pathways in IPA as well as in PANTHER analysis. These results have been validated by real-time PCR and cholesterol assay using scrambled siRNA as a negative control. Similar findings were also observed with human type II pulmonary alveolar epithelial cells, A549. In the present study we have, for the first time, shown the inverse relationship of STAT6 with the cholesterol biosynthesis in lung cancer cells. The present findings are potentially significant to advance the understanding and design of therapeutics for the pathological conditions where both STAT6 and cholesterol biosynthesis are implicated viz. asthma, atherosclerosis etc.</description><subject>Allergies</subject><subject>Alveoli</subject><subject>Analysis</subject><subject>Annexin A5 - pharmacology</subject><subject>Apoptosis</subject><subject>Arteriosclerosis</subject><subject>Asthma</subject><subject>Atherosclerosis</subject><subject>Biology</subject><subject>Biosynthesis</subject><subject>Cancer</subject><subject>Carcinoma - metabolism</subject><subject>Cell death</subject><subject>Cell Line, Tumor</subject><subject>Cholesterol</subject><subject>Cholesterol - chemistry</subject><subject>Cholesterol - metabolism</subject><subject>Computational Biology - methods</subject><subject>Cytokines</subject><subject>Data processing</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA microarrays</subject><subject>Down-Regulation</subject><subject>Epithelial cells</subject><subject>Fluorides</subject><subject>Forkhead Transcription Factors - metabolism</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Silencing</subject><subject>Genes</subject><subject>Genomics</subject><subject>Health aspects</subject><subject>Hepatitis</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Kinases</subject><subject>Lipid metabolism</subject><subject>Lipids</subject><subject>Lung cancer</subject><subject>Lung diseases</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lymphoma</subject><subject>Medicine</subject><subject>Metabolism</subject><subject>Molecular interactions</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Promoter Regions, Genetic</subject><subject>Proteins</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Rodents</subject><subject>siRNA</subject><subject>Stat6 protein</subject><subject>STAT6 Transcription Factor - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dubey, Richa</au><au>Chhabra, Ravindresh</au><au>Saini, Neeru</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Small interfering RNA against transcription factor STAT6 leads to increased cholesterol synthesis in lung cancer cell lines</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2011-12-05</date><risdate>2011</risdate><volume>6</volume><issue>12</issue><spage>e28509</spage><epage>e28509</epage><pages>e28509-e28509</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>STAT6 transcription factor has become a potential molecule for therapeutic intervention because it regulates broad range of cellular processes in a large variety of cell types. Although some target genes and interacting partners of STAT6 have been identified, its exact mechanism of action needs to be elucidated. In this study, we sought to further characterize the molecular interactions, networks, and functions of STAT6 by profiling the mRNA expression of STAT6 silenced human lung cells (NCI-H460) using microarrays. Our analysis revealed 273 differentially expressed genes after STAT6 silencing. Analysis of the gene expression data with Ingenuity Pathway Analysis (IPA) software revealed Gene expression, Cell death, Lipid metabolism as the functions associated with highest rated network. Cholesterol biosynthesis was among the most enriched pathways in IPA as well as in PANTHER analysis. These results have been validated by real-time PCR and cholesterol assay using scrambled siRNA as a negative control. Similar findings were also observed with human type II pulmonary alveolar epithelial cells, A549. In the present study we have, for the first time, shown the inverse relationship of STAT6 with the cholesterol biosynthesis in lung cancer cells. The present findings are potentially significant to advance the understanding and design of therapeutics for the pathological conditions where both STAT6 and cholesterol biosynthesis are implicated viz. asthma, atherosclerosis etc.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22162773</pmid><doi>10.1371/journal.pone.0028509</doi><tpages>e28509</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Allergies Alveoli Analysis Annexin A5 - pharmacology Apoptosis Arteriosclerosis Asthma Atherosclerosis Biology Biosynthesis Cancer Carcinoma - metabolism Cell death Cell Line, Tumor Cholesterol Cholesterol - chemistry Cholesterol - metabolism Computational Biology - methods Cytokines Data processing Deoxyribonucleic acid DNA DNA microarrays Down-Regulation Epithelial cells Fluorides Forkhead Transcription Factors - metabolism Gene expression Gene Expression Profiling Gene Expression Regulation, Neoplastic Gene Silencing Genes Genomics Health aspects Hepatitis Humans Inflammation Kinases Lipid metabolism Lipids Lung cancer Lung diseases Lung Neoplasms - metabolism Lymphoma Medicine Metabolism Molecular interactions Oligonucleotide Array Sequence Analysis Promoter Regions, Genetic Proteins Ribonucleic acid RNA RNA, Small Interfering - metabolism Rodents siRNA Stat6 protein STAT6 Transcription Factor - metabolism Transcription factors Transcription, Genetic Tumor cell lines |
| title | Small interfering RNA against transcription factor STAT6 leads to increased cholesterol synthesis in lung cancer cell lines |
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