Development and molecular characterization of HCT-116 cell lines resistant to the tumor promoter and multiple stress-inducer, deoxycholate
Evidence from live cell bioassays shows that the flat mucosa from patients with colon cancer exhibits resistance to bile salt-induced apoptosis. Three independent cell lines derived from the colonic epithelial cell line HCT-116 were selected for resistance to bile salt-induced apoptosis. These cell...
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| Veröffentlicht in: | Carcinogenesis (New York) 2002-12, Vol.23 (12), p.2063-2080 |
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| creator | Crowley-Weber, Cara L. Payne, Claire M. Gleason-Guzman, Mary Watts, George S. Futscher, Bernard Waltmire, Caroline N. Crowley, Cheray Dvorakova, Katerina Bernstein, Carol Craven, Mary Garewal, Harinder Bernstein, Harris |
| description | Evidence from live cell bioassays shows that the flat mucosa from patients with colon cancer exhibits resistance to bile salt-induced apoptosis. Three independent cell lines derived from the colonic epithelial cell line HCT-116 were selected for resistance to bile salt-induced apoptosis. These cell lines were developed as tissue culture models of apoptosis resistance. Selection was carried out for resistance to apoptosis induced by sodium deoxycholate (NaDOC), the bile salt found in highest concentrations in human fecal water. Cultures of HCT-116 cells were serially passaged in the presence of increasing concentrations of NaDOC. The resulting apoptosis resistant cells were able to grow at concentrations of NaDOC (0.5 mM) that cause apoptosis in a few hours in unselected HCT-116 cells. These cells were then analyzed for changes in gene expression. Observations from cDNA microarray, 2-D gel electrophoresis/MALDI-mass spectroscopy, and confocal microscopy of immunofluorescently stained preparations indicated underexpression or overexpression of numerous genes at either the protein or mRNA level. Genes that may play a role in apoptosis and early stage carcinogenesis have been identified as upregulated in these cell lines, including Grp78, Bcl-2, NF-κB(p50), NF-κB(p65), thioredoxin peroxidase (peroxiredoxin) 2, peroxiredoxin 4, maspin, guanylate cyclase activating protein-1, PKCζ, EGFR, Ras family members, PKA, PI(4,5)K, TRAF2 and BIRC1 (IAP protein). Under-expressed mRNAs included BNIP3, caspase-6, caspase-3 and serine protease 11. NF-κB was constitutively activated in all three resistant cell lines, and was responsible, in part, for the observed apoptosis resistance, determined using antisense oligonucleotide strategies. Molecular and cellular analyses of these resistant cell lines has suggested potential mechanisms by which apoptosis resistance may develop in the colonic epithelium in response to high concentrations of hydrophobic bile acids that are associated with a Western-style diet. These analyses provide the rationale for the development of hypothesis-driven intermediate biomarkers to assess colon cancer risk on an individual basis. |
| doi_str_mv | 10.1093/carcin/23.12.2063 |
| format | Article |
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Three independent cell lines derived from the colonic epithelial cell line HCT-116 were selected for resistance to bile salt-induced apoptosis. These cell lines were developed as tissue culture models of apoptosis resistance. Selection was carried out for resistance to apoptosis induced by sodium deoxycholate (NaDOC), the bile salt found in highest concentrations in human fecal water. Cultures of HCT-116 cells were serially passaged in the presence of increasing concentrations of NaDOC. The resulting apoptosis resistant cells were able to grow at concentrations of NaDOC (0.5 mM) that cause apoptosis in a few hours in unselected HCT-116 cells. These cells were then analyzed for changes in gene expression. Observations from cDNA microarray, 2-D gel electrophoresis/MALDI-mass spectroscopy, and confocal microscopy of immunofluorescently stained preparations indicated underexpression or overexpression of numerous genes at either the protein or mRNA level. Genes that may play a role in apoptosis and early stage carcinogenesis have been identified as upregulated in these cell lines, including Grp78, Bcl-2, NF-κB(p50), NF-κB(p65), thioredoxin peroxidase (peroxiredoxin) 2, peroxiredoxin 4, maspin, guanylate cyclase activating protein-1, PKCζ, EGFR, Ras family members, PKA, PI(4,5)K, TRAF2 and BIRC1 (IAP protein). Under-expressed mRNAs included BNIP3, caspase-6, caspase-3 and serine protease 11. NF-κB was constitutively activated in all three resistant cell lines, and was responsible, in part, for the observed apoptosis resistance, determined using antisense oligonucleotide strategies. Molecular and cellular analyses of these resistant cell lines has suggested potential mechanisms by which apoptosis resistance may develop in the colonic epithelium in response to high concentrations of hydrophobic bile acids that are associated with a Western-style diet. These analyses provide the rationale for the development of hypothesis-driven intermediate biomarkers to assess colon cancer risk on an individual basis.</description><identifier>ISSN: 0143-3334</identifier><identifier>ISSN: 1460-2180</identifier><identifier>EISSN: 1460-2180</identifier><identifier>DOI: 10.1093/carcin/23.12.2063</identifier><identifier>PMID: 12507930</identifier><identifier>CODEN: CRNGDP</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>78 kD-glucose-regulated protein ; Apoptosis ; Bcl2/adenovirus EIB 19 kD-interacting protein 3 ; BH4 ; Biological and medical sciences ; BNIP3 ; calcium/calmodulin-dependent protein kinase II delta ; CAMK2D ; Carcinogenesis, carcinogens and anticarcinogens ; Carrier Proteins - metabolism ; cGMP-activated protein kinase ; Chemical agents ; Colon - metabolism ; deoxycholate ; Deoxycholic Acid - pharmacology ; Detergents - pharmacology ; DHAP ; dihydroxyacetone phosphate ; DNA, Complementary - metabolism ; DOC ; Down-Regulation ; Drug Resistance, Neoplasm ; EGFR ; Electrophoresis, Gel, Two-Dimensional ; endoplasmic reticulum ; epidermal growth factor receptor ; Epithelial Cells ; GAP ; glyceraldehyde 3-phosphate ; Grp78 ; guanylate cyclase ; Heat-Shock Proteins ; Humans ; IAP ; IEF ; IKK-β ; inducible NO synthase ; inhibitor of apoptosis protein ; inositol triphosphate ; IP3 ; isoelectric focusing ; IκB-kinase-β ; Lysosomes - metabolism ; MALDI-MS ; MAPK ; MAPK kinase ; matrix assisted laser desorption ionization mass spectroscopy ; Medical sciences ; MEK ; MEK kinase ; MEKK ; Microscopy, Confocal ; Microscopy, Electron ; Microscopy, Fluorescence ; Mitochondria - metabolism ; mitogen-activated protein kinase ; Models, Biological ; Molecular Chaperones - metabolism ; NaDOC ; NF-kappa B - metabolism ; NF-kappa B p50 Subunit ; NF-κB-inducing kinase ; NIK ; nitric oxide ; NLS ; NOS2 ; nuclear localization signal ; Oligonucleotide Array Sequence Analysis ; Oligonucleotides - pharmacology ; Oligonucleotides, Antisense - pharmacology ; ONOO ; Oxidative Stress ; PDTC ; peroxynitrite ; PKCζ ; PKG ; PN-1 ; Promoter Regions, Genetic ; protease nexin-1 ; protein kinase C-zeta ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; pyrrolidine dithiocarbamate ; QDPR ; quinoid dihydropteridine reductase ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - metabolism ; serine protease inhibitor ; SERPIN ; sodium deoxycholate ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; TEM ; tetrahydrobiopterin ; thenoyl trifluoroacetone ; thioredoxin ; TPI ; TPx ; TRAF ; Transcription Factor RelA ; transmission electron microscopy ; triose phosphate isomerase ; Trx ; Trx peroxidase (peroxiredoxin) ; Trx reductase ; TTFA ; Tumor Cells, Cultured ; tumor necrosis factor receptor-associated factor ; Tumors ; Up-Regulation</subject><ispartof>Carcinogenesis (New York), 2002-12, Vol.23 (12), p.2063-2080</ispartof><rights>2003 INIST-CNRS</rights><rights>Copyright Oxford University Press(England) Dec 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c435t-3a64c4bf5624306fe05ba49f58e6c6b079aaecf1f38426fb66055263a7869c2d3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14465317$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12507930$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Crowley-Weber, Cara L.</creatorcontrib><creatorcontrib>Payne, Claire M.</creatorcontrib><creatorcontrib>Gleason-Guzman, Mary</creatorcontrib><creatorcontrib>Watts, George S.</creatorcontrib><creatorcontrib>Futscher, Bernard</creatorcontrib><creatorcontrib>Waltmire, Caroline N.</creatorcontrib><creatorcontrib>Crowley, Cheray</creatorcontrib><creatorcontrib>Dvorakova, Katerina</creatorcontrib><creatorcontrib>Bernstein, Carol</creatorcontrib><creatorcontrib>Craven, Mary</creatorcontrib><creatorcontrib>Garewal, Harinder</creatorcontrib><creatorcontrib>Bernstein, Harris</creatorcontrib><title>Development and molecular characterization of HCT-116 cell lines resistant to the tumor promoter and multiple stress-inducer, deoxycholate</title><title>Carcinogenesis (New York)</title><addtitle>Carcinogenesis</addtitle><description>Evidence from live cell bioassays shows that the flat mucosa from patients with colon cancer exhibits resistance to bile salt-induced apoptosis. Three independent cell lines derived from the colonic epithelial cell line HCT-116 were selected for resistance to bile salt-induced apoptosis. These cell lines were developed as tissue culture models of apoptosis resistance. Selection was carried out for resistance to apoptosis induced by sodium deoxycholate (NaDOC), the bile salt found in highest concentrations in human fecal water. Cultures of HCT-116 cells were serially passaged in the presence of increasing concentrations of NaDOC. The resulting apoptosis resistant cells were able to grow at concentrations of NaDOC (0.5 mM) that cause apoptosis in a few hours in unselected HCT-116 cells. These cells were then analyzed for changes in gene expression. Observations from cDNA microarray, 2-D gel electrophoresis/MALDI-mass spectroscopy, and confocal microscopy of immunofluorescently stained preparations indicated underexpression or overexpression of numerous genes at either the protein or mRNA level. Genes that may play a role in apoptosis and early stage carcinogenesis have been identified as upregulated in these cell lines, including Grp78, Bcl-2, NF-κB(p50), NF-κB(p65), thioredoxin peroxidase (peroxiredoxin) 2, peroxiredoxin 4, maspin, guanylate cyclase activating protein-1, PKCζ, EGFR, Ras family members, PKA, PI(4,5)K, TRAF2 and BIRC1 (IAP protein). Under-expressed mRNAs included BNIP3, caspase-6, caspase-3 and serine protease 11. NF-κB was constitutively activated in all three resistant cell lines, and was responsible, in part, for the observed apoptosis resistance, determined using antisense oligonucleotide strategies. Molecular and cellular analyses of these resistant cell lines has suggested potential mechanisms by which apoptosis resistance may develop in the colonic epithelium in response to high concentrations of hydrophobic bile acids that are associated with a Western-style diet. These analyses provide the rationale for the development of hypothesis-driven intermediate biomarkers to assess colon cancer risk on an individual basis.</description><subject>78 kD-glucose-regulated protein</subject><subject>Apoptosis</subject><subject>Bcl2/adenovirus EIB 19 kD-interacting protein 3</subject><subject>BH4</subject><subject>Biological and medical sciences</subject><subject>BNIP3</subject><subject>calcium/calmodulin-dependent protein kinase II delta</subject><subject>CAMK2D</subject><subject>Carcinogenesis, carcinogens and anticarcinogens</subject><subject>Carrier Proteins - metabolism</subject><subject>cGMP-activated protein kinase</subject><subject>Chemical agents</subject><subject>Colon - metabolism</subject><subject>deoxycholate</subject><subject>Deoxycholic Acid - pharmacology</subject><subject>Detergents - pharmacology</subject><subject>DHAP</subject><subject>dihydroxyacetone phosphate</subject><subject>DNA, Complementary - metabolism</subject><subject>DOC</subject><subject>Down-Regulation</subject><subject>Drug Resistance, Neoplasm</subject><subject>EGFR</subject><subject>Electrophoresis, Gel, Two-Dimensional</subject><subject>endoplasmic reticulum</subject><subject>epidermal growth factor receptor</subject><subject>Epithelial Cells</subject><subject>GAP</subject><subject>glyceraldehyde 3-phosphate</subject><subject>Grp78</subject><subject>guanylate cyclase</subject><subject>Heat-Shock Proteins</subject><subject>Humans</subject><subject>IAP</subject><subject>IEF</subject><subject>IKK-β</subject><subject>inducible NO synthase</subject><subject>inhibitor of apoptosis protein</subject><subject>inositol triphosphate</subject><subject>IP3</subject><subject>isoelectric focusing</subject><subject>IκB-kinase-β</subject><subject>Lysosomes - metabolism</subject><subject>MALDI-MS</subject><subject>MAPK</subject><subject>MAPK kinase</subject><subject>matrix assisted laser desorption ionization mass spectroscopy</subject><subject>Medical sciences</subject><subject>MEK</subject><subject>MEK kinase</subject><subject>MEKK</subject><subject>Microscopy, Confocal</subject><subject>Microscopy, Electron</subject><subject>Microscopy, Fluorescence</subject><subject>Mitochondria - metabolism</subject><subject>mitogen-activated protein kinase</subject><subject>Models, Biological</subject><subject>Molecular Chaperones - metabolism</subject><subject>NaDOC</subject><subject>NF-kappa B - metabolism</subject><subject>NF-kappa B p50 Subunit</subject><subject>NF-κB-inducing kinase</subject><subject>NIK</subject><subject>nitric oxide</subject><subject>NLS</subject><subject>NOS2</subject><subject>nuclear localization signal</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Oligonucleotides - pharmacology</subject><subject>Oligonucleotides, Antisense - pharmacology</subject><subject>ONOO</subject><subject>Oxidative Stress</subject><subject>PDTC</subject><subject>peroxynitrite</subject><subject>PKCζ</subject><subject>PKG</subject><subject>PN-1</subject><subject>Promoter Regions, Genetic</subject><subject>protease nexin-1</subject><subject>protein kinase C-zeta</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>pyrrolidine dithiocarbamate</subject><subject>QDPR</subject><subject>quinoid dihydropteridine reductase</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - metabolism</subject><subject>serine protease inhibitor</subject><subject>SERPIN</subject><subject>sodium deoxycholate</subject><subject>Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization</subject><subject>TEM</subject><subject>tetrahydrobiopterin</subject><subject>thenoyl trifluoroacetone</subject><subject>thioredoxin</subject><subject>TPI</subject><subject>TPx</subject><subject>TRAF</subject><subject>Transcription Factor RelA</subject><subject>transmission electron microscopy</subject><subject>triose phosphate isomerase</subject><subject>Trx</subject><subject>Trx peroxidase (peroxiredoxin)</subject><subject>Trx reductase</subject><subject>TTFA</subject><subject>Tumor Cells, Cultured</subject><subject>tumor necrosis factor receptor-associated factor</subject><subject>Tumors</subject><subject>Up-Regulation</subject><issn>0143-3334</issn><issn>1460-2180</issn><issn>1460-2180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkMFu1DAURSMEokPhA9ggC4ldM7X9bGeyhKEwoCI2RarYWI7zrElx4qntoJZP4KtxlRFdWG_hc--zT1W9ZnTNaAvn1kQ7TOcc1oyvOVXwpFoxoWjN2YY-rVaUCagBQJxUL1K6oZQpkO3z6oRxSZsW6Kr6-xF_ow-HEadMzNSTMXi0szeR2L2JxmaMwx-ThzCR4Mhue1UzpohF74kfJkwkYhpSNiWeA8l7JHkeQySHGMZQwkvp7PNw8EhSLniqh6mfLcYz0mO4u7f74E3Gl9UzZ3zCV8d5Wv34dHG13dWX3z9_2b6_rK0AmWswSljROam4AKocUtkZ0Tq5QWVVV_5lDFrHHGwEV65TikrJFZhmo1rLezit3i695Ym3M6asb8Icp7JSc9aClMVTgdgC2RhSiuj0IQ6jifeaUf0gXy_yNQfNuH6QXzJvjsVzN2L_mDjaLsC7I2CSNd5FM9khPXJCKAmsKVy9cEUs3v2_N_GXVg00Uu-uf5bzlX_4Jq-1gH_AtZ9D</recordid><startdate>20021201</startdate><enddate>20021201</enddate><creator>Crowley-Weber, Cara L.</creator><creator>Payne, Claire M.</creator><creator>Gleason-Guzman, Mary</creator><creator>Watts, George S.</creator><creator>Futscher, Bernard</creator><creator>Waltmire, Caroline N.</creator><creator>Crowley, Cheray</creator><creator>Dvorakova, Katerina</creator><creator>Bernstein, Carol</creator><creator>Craven, Mary</creator><creator>Garewal, Harinder</creator><creator>Bernstein, Harris</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>BSCLL</scope><scope>IQODW</scope><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>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20021201</creationdate><title>Development and molecular characterization of HCT-116 cell lines resistant to the tumor promoter and multiple stress-inducer, deoxycholate</title><author>Crowley-Weber, Cara L. ; Payne, Claire M. ; Gleason-Guzman, Mary ; Watts, George S. ; Futscher, Bernard ; Waltmire, Caroline N. ; Crowley, Cheray ; Dvorakova, Katerina ; Bernstein, Carol ; Craven, Mary ; Garewal, Harinder ; Bernstein, Harris</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c435t-3a64c4bf5624306fe05ba49f58e6c6b079aaecf1f38426fb66055263a7869c2d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>78 kD-glucose-regulated protein</topic><topic>Apoptosis</topic><topic>Bcl2/adenovirus EIB 19 kD-interacting protein 3</topic><topic>BH4</topic><topic>Biological and medical sciences</topic><topic>BNIP3</topic><topic>calcium/calmodulin-dependent protein kinase II delta</topic><topic>CAMK2D</topic><topic>Carcinogenesis, carcinogens and anticarcinogens</topic><topic>Carrier Proteins - metabolism</topic><topic>cGMP-activated protein kinase</topic><topic>Chemical agents</topic><topic>Colon - metabolism</topic><topic>deoxycholate</topic><topic>Deoxycholic Acid - pharmacology</topic><topic>Detergents - pharmacology</topic><topic>DHAP</topic><topic>dihydroxyacetone phosphate</topic><topic>DNA, Complementary - metabolism</topic><topic>DOC</topic><topic>Down-Regulation</topic><topic>Drug Resistance, Neoplasm</topic><topic>EGFR</topic><topic>Electrophoresis, Gel, Two-Dimensional</topic><topic>endoplasmic reticulum</topic><topic>epidermal growth factor receptor</topic><topic>Epithelial Cells</topic><topic>GAP</topic><topic>glyceraldehyde 3-phosphate</topic><topic>Grp78</topic><topic>guanylate cyclase</topic><topic>Heat-Shock Proteins</topic><topic>Humans</topic><topic>IAP</topic><topic>IEF</topic><topic>IKK-β</topic><topic>inducible NO synthase</topic><topic>inhibitor of apoptosis protein</topic><topic>inositol triphosphate</topic><topic>IP3</topic><topic>isoelectric focusing</topic><topic>IκB-kinase-β</topic><topic>Lysosomes - metabolism</topic><topic>MALDI-MS</topic><topic>MAPK</topic><topic>MAPK kinase</topic><topic>matrix assisted laser desorption ionization mass spectroscopy</topic><topic>Medical sciences</topic><topic>MEK</topic><topic>MEK kinase</topic><topic>MEKK</topic><topic>Microscopy, Confocal</topic><topic>Microscopy, Electron</topic><topic>Microscopy, Fluorescence</topic><topic>Mitochondria - metabolism</topic><topic>mitogen-activated protein kinase</topic><topic>Models, Biological</topic><topic>Molecular Chaperones - metabolism</topic><topic>NaDOC</topic><topic>NF-kappa B - metabolism</topic><topic>NF-kappa B p50 Subunit</topic><topic>NF-κB-inducing kinase</topic><topic>NIK</topic><topic>nitric oxide</topic><topic>NLS</topic><topic>NOS2</topic><topic>nuclear localization signal</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Oligonucleotides - pharmacology</topic><topic>Oligonucleotides, Antisense - pharmacology</topic><topic>ONOO</topic><topic>Oxidative Stress</topic><topic>PDTC</topic><topic>peroxynitrite</topic><topic>PKCζ</topic><topic>PKG</topic><topic>PN-1</topic><topic>Promoter Regions, Genetic</topic><topic>protease nexin-1</topic><topic>protein kinase C-zeta</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>pyrrolidine dithiocarbamate</topic><topic>QDPR</topic><topic>quinoid dihydropteridine reductase</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - metabolism</topic><topic>serine protease inhibitor</topic><topic>SERPIN</topic><topic>sodium deoxycholate</topic><topic>Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization</topic><topic>TEM</topic><topic>tetrahydrobiopterin</topic><topic>thenoyl trifluoroacetone</topic><topic>thioredoxin</topic><topic>TPI</topic><topic>TPx</topic><topic>TRAF</topic><topic>Transcription Factor RelA</topic><topic>transmission electron microscopy</topic><topic>triose phosphate isomerase</topic><topic>Trx</topic><topic>Trx peroxidase (peroxiredoxin)</topic><topic>Trx reductase</topic><topic>TTFA</topic><topic>Tumor Cells, Cultured</topic><topic>tumor necrosis factor receptor-associated factor</topic><topic>Tumors</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Crowley-Weber, Cara L.</creatorcontrib><creatorcontrib>Payne, Claire M.</creatorcontrib><creatorcontrib>Gleason-Guzman, Mary</creatorcontrib><creatorcontrib>Watts, George S.</creatorcontrib><creatorcontrib>Futscher, Bernard</creatorcontrib><creatorcontrib>Waltmire, Caroline N.</creatorcontrib><creatorcontrib>Crowley, Cheray</creatorcontrib><creatorcontrib>Dvorakova, Katerina</creatorcontrib><creatorcontrib>Bernstein, Carol</creatorcontrib><creatorcontrib>Craven, Mary</creatorcontrib><creatorcontrib>Garewal, Harinder</creatorcontrib><creatorcontrib>Bernstein, Harris</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Carcinogenesis (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Crowley-Weber, Cara L.</au><au>Payne, Claire M.</au><au>Gleason-Guzman, Mary</au><au>Watts, George S.</au><au>Futscher, Bernard</au><au>Waltmire, Caroline N.</au><au>Crowley, Cheray</au><au>Dvorakova, Katerina</au><au>Bernstein, Carol</au><au>Craven, Mary</au><au>Garewal, Harinder</au><au>Bernstein, Harris</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Development and molecular characterization of HCT-116 cell lines resistant to the tumor promoter and multiple stress-inducer, deoxycholate</atitle><jtitle>Carcinogenesis (New York)</jtitle><addtitle>Carcinogenesis</addtitle><date>2002-12-01</date><risdate>2002</risdate><volume>23</volume><issue>12</issue><spage>2063</spage><epage>2080</epage><pages>2063-2080</pages><issn>0143-3334</issn><issn>1460-2180</issn><eissn>1460-2180</eissn><coden>CRNGDP</coden><abstract>Evidence from live cell bioassays shows that the flat mucosa from patients with colon cancer exhibits resistance to bile salt-induced apoptosis. Three independent cell lines derived from the colonic epithelial cell line HCT-116 were selected for resistance to bile salt-induced apoptosis. These cell lines were developed as tissue culture models of apoptosis resistance. Selection was carried out for resistance to apoptosis induced by sodium deoxycholate (NaDOC), the bile salt found in highest concentrations in human fecal water. Cultures of HCT-116 cells were serially passaged in the presence of increasing concentrations of NaDOC. The resulting apoptosis resistant cells were able to grow at concentrations of NaDOC (0.5 mM) that cause apoptosis in a few hours in unselected HCT-116 cells. These cells were then analyzed for changes in gene expression. Observations from cDNA microarray, 2-D gel electrophoresis/MALDI-mass spectroscopy, and confocal microscopy of immunofluorescently stained preparations indicated underexpression or overexpression of numerous genes at either the protein or mRNA level. Genes that may play a role in apoptosis and early stage carcinogenesis have been identified as upregulated in these cell lines, including Grp78, Bcl-2, NF-κB(p50), NF-κB(p65), thioredoxin peroxidase (peroxiredoxin) 2, peroxiredoxin 4, maspin, guanylate cyclase activating protein-1, PKCζ, EGFR, Ras family members, PKA, PI(4,5)K, TRAF2 and BIRC1 (IAP protein). Under-expressed mRNAs included BNIP3, caspase-6, caspase-3 and serine protease 11. NF-κB was constitutively activated in all three resistant cell lines, and was responsible, in part, for the observed apoptosis resistance, determined using antisense oligonucleotide strategies. Molecular and cellular analyses of these resistant cell lines has suggested potential mechanisms by which apoptosis resistance may develop in the colonic epithelium in response to high concentrations of hydrophobic bile acids that are associated with a Western-style diet. These analyses provide the rationale for the development of hypothesis-driven intermediate biomarkers to assess colon cancer risk on an individual basis.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>12507930</pmid><doi>10.1093/carcin/23.12.2063</doi><tpages>18</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0143-3334 |
| ispartof | Carcinogenesis (New York), 2002-12, Vol.23 (12), p.2063-2080 |
| issn | 0143-3334 1460-2180 1460-2180 |
| language | eng |
| recordid | cdi_proquest_journals_219355001 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Oxford University Press Journals All Titles (1996-Current); Alma/SFX Local Collection |
| subjects | 78 kD-glucose-regulated protein Apoptosis Bcl2/adenovirus EIB 19 kD-interacting protein 3 BH4 Biological and medical sciences BNIP3 calcium/calmodulin-dependent protein kinase II delta CAMK2D Carcinogenesis, carcinogens and anticarcinogens Carrier Proteins - metabolism cGMP-activated protein kinase Chemical agents Colon - metabolism deoxycholate Deoxycholic Acid - pharmacology Detergents - pharmacology DHAP dihydroxyacetone phosphate DNA, Complementary - metabolism DOC Down-Regulation Drug Resistance, Neoplasm EGFR Electrophoresis, Gel, Two-Dimensional endoplasmic reticulum epidermal growth factor receptor Epithelial Cells GAP glyceraldehyde 3-phosphate Grp78 guanylate cyclase Heat-Shock Proteins Humans IAP IEF IKK-β inducible NO synthase inhibitor of apoptosis protein inositol triphosphate IP3 isoelectric focusing IκB-kinase-β Lysosomes - metabolism MALDI-MS MAPK MAPK kinase matrix assisted laser desorption ionization mass spectroscopy Medical sciences MEK MEK kinase MEKK Microscopy, Confocal Microscopy, Electron Microscopy, Fluorescence Mitochondria - metabolism mitogen-activated protein kinase Models, Biological Molecular Chaperones - metabolism NaDOC NF-kappa B - metabolism NF-kappa B p50 Subunit NF-κB-inducing kinase NIK nitric oxide NLS NOS2 nuclear localization signal Oligonucleotide Array Sequence Analysis Oligonucleotides - pharmacology Oligonucleotides, Antisense - pharmacology ONOO Oxidative Stress PDTC peroxynitrite PKCζ PKG PN-1 Promoter Regions, Genetic protease nexin-1 protein kinase C-zeta Proto-Oncogene Proteins c-bcl-2 - metabolism pyrrolidine dithiocarbamate QDPR quinoid dihydropteridine reductase Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - metabolism serine protease inhibitor SERPIN sodium deoxycholate Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization TEM tetrahydrobiopterin thenoyl trifluoroacetone thioredoxin TPI TPx TRAF Transcription Factor RelA transmission electron microscopy triose phosphate isomerase Trx Trx peroxidase (peroxiredoxin) Trx reductase TTFA Tumor Cells, Cultured tumor necrosis factor receptor-associated factor Tumors Up-Regulation |
| title | Development and molecular characterization of HCT-116 cell lines resistant to the tumor promoter and multiple stress-inducer, deoxycholate |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-26T21%3A59%3A28IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Development%20and%20molecular%20characterization%20of%20HCT-116%20cell%20lines%20resistant%20to%20the%20tumor%20promoter%20and%20multiple%20stress-inducer,%20deoxycholate&rft.jtitle=Carcinogenesis%20(New%20York)&rft.au=Crowley-Weber,%20Cara%20L.&rft.date=2002-12-01&rft.volume=23&rft.issue=12&rft.spage=2063&rft.epage=2080&rft.pages=2063-2080&rft.issn=0143-3334&rft.eissn=1460-2180&rft.coden=CRNGDP&rft_id=info:doi/10.1093/carcin/23.12.2063&rft_dat=%3Cproquest_cross%3E347638111%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=219355001&rft_id=info:pmid/12507930&rfr_iscdi=true |