Fatty acid synthase expression and esophageal cancer
Fatty acid synthase (FASN) overexpression has also been associated with a variety of human malignancies including tumor progression, aggressiveness, and metastasis. To investigate the role of FASN expression in esophageal cancer, we evaluated 60 cases of squamous cell carcinoma, 20 cases of adenocar...
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Veröffentlicht in: | Molecular biology reports 2012-10, Vol.39 (10), p.9733-9739 |
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description | Fatty acid synthase (FASN) overexpression has also been associated with a variety of human malignancies including tumor progression, aggressiveness, and metastasis. To investigate the role of FASN expression in esophageal cancer, we evaluated 60 cases of squamous cell carcinoma, 20 cases of adenocarcinoma, and 10 cases of normal esophageal tissues. We found that FASN was detected in 95 % human squamous cell carcinoma, and in 90 % human adenocarcinoma samples. However, all cases of normal esophageal epithelium did not express the protein of FASN. Further, to investigate the role of FASN in tumorigenesis and development, we analyze the growth and migration by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation and wound healing assay. We found that inhibition of FASN expression in TE13 cells by RNAi suppressed the growth of cells. Decreased FASN expression mitigated the migration of TE13 cells. These studies demonstrated the functional importance of FASN in esophageal tumorigenesis, and suggested that inhibiting FASN might be applied to treat esophageal cancer. |
doi_str_mv | 10.1007/s11033-012-1838-y |
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To investigate the role of FASN expression in esophageal cancer, we evaluated 60 cases of squamous cell carcinoma, 20 cases of adenocarcinoma, and 10 cases of normal esophageal tissues. We found that FASN was detected in 95 % human squamous cell carcinoma, and in 90 % human adenocarcinoma samples. However, all cases of normal esophageal epithelium did not express the protein of FASN. Further, to investigate the role of FASN in tumorigenesis and development, we analyze the growth and migration by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation and wound healing assay. We found that inhibition of FASN expression in TE13 cells by RNAi suppressed the growth of cells. Decreased FASN expression mitigated the migration of TE13 cells. These studies demonstrated the functional importance of FASN in esophageal tumorigenesis, and suggested that inhibiting FASN might be applied to treat esophageal cancer.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-012-1838-y</identifier><identifier>PMID: 22723001</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Adenocarcinoma - enzymology ; Animal Anatomy ; Animal Biochemistry ; Biomedical and Life Sciences ; Cancer ; Carcinoma, Squamous Cell - enzymology ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Enzymes ; Esophageal Neoplasms - enzymology ; Esophagus ; Esophagus - enzymology ; Esophagus - pathology ; Fatty Acid Synthase, Type I - genetics ; Fatty Acid Synthase, Type I - metabolism ; Fatty acids ; Female ; Gene Expression ; Gene Knockdown Techniques ; Histology ; Humans ; Immunohistochemistry ; Life Sciences ; Male ; Metastasis ; Middle Aged ; Morphology ; Mucous Membrane - enzymology ; RNA Interference ; Tumors</subject><ispartof>Molecular biology reports, 2012-10, Vol.39 (10), p.9733-9739</ispartof><rights>Springer Science+Business Media B.V. 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-eaeddba251b4d2ac6cc9697d1df527b898605e4ce0753f369ab96a92fba9b0083</citedby><cites>FETCH-LOGICAL-c372t-eaeddba251b4d2ac6cc9697d1df527b898605e4ce0753f369ab96a92fba9b0083</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11033-012-1838-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11033-012-1838-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22723001$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Yongli</creatorcontrib><creatorcontrib>Niu, Chunyan</creatorcontrib><creatorcontrib>Li, Yandong</creatorcontrib><creatorcontrib>Gao, Baohua</creatorcontrib><creatorcontrib>Zheng, Jianyun</creatorcontrib><creatorcontrib>Guo, Xiaoli</creatorcontrib><creatorcontrib>Ma, Weiguo</creatorcontrib><title>Fatty acid synthase expression and esophageal cancer</title><title>Molecular biology reports</title><addtitle>Mol Biol Rep</addtitle><addtitle>Mol Biol Rep</addtitle><description>Fatty acid synthase (FASN) overexpression has also been associated with a variety of human malignancies including tumor progression, aggressiveness, and metastasis. To investigate the role of FASN expression in esophageal cancer, we evaluated 60 cases of squamous cell carcinoma, 20 cases of adenocarcinoma, and 10 cases of normal esophageal tissues. We found that FASN was detected in 95 % human squamous cell carcinoma, and in 90 % human adenocarcinoma samples. However, all cases of normal esophageal epithelium did not express the protein of FASN. Further, to investigate the role of FASN in tumorigenesis and development, we analyze the growth and migration by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation and wound healing assay. We found that inhibition of FASN expression in TE13 cells by RNAi suppressed the growth of cells. Decreased FASN expression mitigated the migration of TE13 cells. These studies demonstrated the functional importance of FASN in esophageal tumorigenesis, and suggested that inhibiting FASN might be applied to treat esophageal cancer.</description><subject>Adenocarcinoma - enzymology</subject><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cancer</subject><subject>Carcinoma, Squamous Cell - enzymology</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Enzymes</subject><subject>Esophageal Neoplasms - enzymology</subject><subject>Esophagus</subject><subject>Esophagus - enzymology</subject><subject>Esophagus - pathology</subject><subject>Fatty Acid Synthase, Type I - genetics</subject><subject>Fatty Acid Synthase, Type I - metabolism</subject><subject>Fatty acids</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Gene Knockdown Techniques</subject><subject>Histology</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Metastasis</subject><subject>Middle Aged</subject><subject>Morphology</subject><subject>Mucous Membrane - 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enzymology</topic><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cancer</topic><topic>Carcinoma, Squamous Cell - enzymology</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Enzymes</topic><topic>Esophageal Neoplasms - enzymology</topic><topic>Esophagus</topic><topic>Esophagus - enzymology</topic><topic>Esophagus - pathology</topic><topic>Fatty Acid Synthase, Type I - genetics</topic><topic>Fatty Acid Synthase, Type I - metabolism</topic><topic>Fatty acids</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Gene Knockdown Techniques</topic><topic>Histology</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Metastasis</topic><topic>Middle Aged</topic><topic>Morphology</topic><topic>Mucous Membrane - enzymology</topic><topic>RNA Interference</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Yongli</creatorcontrib><creatorcontrib>Niu, Chunyan</creatorcontrib><creatorcontrib>Li, Yandong</creatorcontrib><creatorcontrib>Gao, Baohua</creatorcontrib><creatorcontrib>Zheng, Jianyun</creatorcontrib><creatorcontrib>Guo, Xiaoli</creatorcontrib><creatorcontrib>Ma, Weiguo</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>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular biology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Yongli</au><au>Niu, Chunyan</au><au>Li, Yandong</au><au>Gao, Baohua</au><au>Zheng, Jianyun</au><au>Guo, Xiaoli</au><au>Ma, Weiguo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fatty acid synthase expression and esophageal cancer</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><addtitle>Mol Biol Rep</addtitle><date>2012-10-01</date><risdate>2012</risdate><volume>39</volume><issue>10</issue><spage>9733</spage><epage>9739</epage><pages>9733-9739</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>Fatty acid synthase (FASN) overexpression has also been associated with a variety of human malignancies including tumor progression, aggressiveness, and metastasis. To investigate the role of FASN expression in esophageal cancer, we evaluated 60 cases of squamous cell carcinoma, 20 cases of adenocarcinoma, and 10 cases of normal esophageal tissues. We found that FASN was detected in 95 % human squamous cell carcinoma, and in 90 % human adenocarcinoma samples. However, all cases of normal esophageal epithelium did not express the protein of FASN. Further, to investigate the role of FASN in tumorigenesis and development, we analyze the growth and migration by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation and wound healing assay. We found that inhibition of FASN expression in TE13 cells by RNAi suppressed the growth of cells. Decreased FASN expression mitigated the migration of TE13 cells. These studies demonstrated the functional importance of FASN in esophageal tumorigenesis, and suggested that inhibiting FASN might be applied to treat esophageal cancer.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>22723001</pmid><doi>10.1007/s11033-012-1838-y</doi><tpages>7</tpages></addata></record> |
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subjects | Adenocarcinoma - enzymology Animal Anatomy Animal Biochemistry Biomedical and Life Sciences Cancer Carcinoma, Squamous Cell - enzymology Cell Line, Tumor Cell Movement Cell Proliferation Enzymes Esophageal Neoplasms - enzymology Esophagus Esophagus - enzymology Esophagus - pathology Fatty Acid Synthase, Type I - genetics Fatty Acid Synthase, Type I - metabolism Fatty acids Female Gene Expression Gene Knockdown Techniques Histology Humans Immunohistochemistry Life Sciences Male Metastasis Middle Aged Morphology Mucous Membrane - enzymology RNA Interference Tumors |
title | Fatty acid synthase expression and esophageal cancer |
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