Hedgehog pathway signaling regulates human colon carcinoma HT-29 epithelial cell line apoptosis and cytokine secretion
The Hedgehog (Hh) pathway is involved in embryogenesis and physiologic processes including cell survival and proliferation. We used the HT-29 and other human colon carcinoma cell lines to investigate Hh signaling and biological functions in colonic epithelial cells. HT-29 cells were cultured under d...
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| Veröffentlicht in: | PloS one 2012-09, Vol.7 (9), p.e45332 |
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| description | The Hedgehog (Hh) pathway is involved in embryogenesis and physiologic processes including cell survival and proliferation. We used the HT-29 and other human colon carcinoma cell lines to investigate Hh signaling and biological functions in colonic epithelial cells. HT-29 cells were cultured under different conditions and exposed to various stimuli. The expression of Hh pathway components and related genes and proteins were assessed by real-time PCR and immunofluorescence. Viability, apoptosis and cell proliferation were measured by the MTT assay, Annexin-V/7-AAD staining and BrdU uptake, respectively. Chemokines production was measured by ELISA in culture supernatants. Indian and Sonic Hh mRNA levels and the downstream transcription factors Gli-1 and Gli-2 increased following treatment with Hh agonists and butyrate, but decreased upon exposure to cyclopamine or GANT61. BMP4 and BMP7 expression increased after stimulation with Hh agonists. Gli-1 protein expression increased after Hh agonists and decreased following cyclopamine. Exposure to Hh agonists promoted β-catenin reduction and subcellular redistribution. Levels of IL-8 and MCP-1 decreased upon exposure to Hh agonists compared to Hh antagonists, LPS, IFN-γ or EGF. Monocyte chemotaxis decreased upon exposure to supernatants of HT-29 cells treated with Shh compared to Hh antagonists, LPS and IFN-γ. Cellular incorporation of BrdU and cell viability decreased following Hh blockade. Hh agonists abrogated the anti-CD95 induced apoptosis. Hh pathway is a key controller of colon cancer cells, as demonstrated by its effect in dampening inflammatory signals and antagonizing apoptosis. The differential expression of Hh components may underlie abnormalities in the local immune response and in epithelial barrier integrity, with potential homeostatic implications for the development of colonic inflammation and malignancies. |
| doi_str_mv | 10.1371/journal.pone.0045332 |
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We used the HT-29 and other human colon carcinoma cell lines to investigate Hh signaling and biological functions in colonic epithelial cells. HT-29 cells were cultured under different conditions and exposed to various stimuli. The expression of Hh pathway components and related genes and proteins were assessed by real-time PCR and immunofluorescence. Viability, apoptosis and cell proliferation were measured by the MTT assay, Annexin-V/7-AAD staining and BrdU uptake, respectively. Chemokines production was measured by ELISA in culture supernatants. Indian and Sonic Hh mRNA levels and the downstream transcription factors Gli-1 and Gli-2 increased following treatment with Hh agonists and butyrate, but decreased upon exposure to cyclopamine or GANT61. BMP4 and BMP7 expression increased after stimulation with Hh agonists. Gli-1 protein expression increased after Hh agonists and decreased following cyclopamine. Exposure to Hh agonists promoted β-catenin reduction and subcellular redistribution. Levels of IL-8 and MCP-1 decreased upon exposure to Hh agonists compared to Hh antagonists, LPS, IFN-γ or EGF. Monocyte chemotaxis decreased upon exposure to supernatants of HT-29 cells treated with Shh compared to Hh antagonists, LPS and IFN-γ. Cellular incorporation of BrdU and cell viability decreased following Hh blockade. Hh agonists abrogated the anti-CD95 induced apoptosis. Hh pathway is a key controller of colon cancer cells, as demonstrated by its effect in dampening inflammatory signals and antagonizing apoptosis. The differential expression of Hh components may underlie abnormalities in the local immune response and in epithelial barrier integrity, with potential homeostatic implications for the development of colonic inflammation and malignancies.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0045332</identifier><identifier>PMID: 23028941</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Abnormalities ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - genetics ; beta Catenin - genetics ; beta Catenin - metabolism ; Biology ; Bone Morphogenetic Protein 4 - genetics ; Bone Morphogenetic Protein 4 - metabolism ; Bone Morphogenetic Protein 7 - genetics ; Bone Morphogenetic Protein 7 - metabolism ; Breast cancer ; Butyrates - pharmacology ; CD95 antigen ; Cell culture ; Cell cycle ; Cell proliferation ; Cell survival ; Cell Survival - drug effects ; Cell Survival - genetics ; Chemokine CCL2 - genetics ; Chemokine CCL2 - metabolism ; Chemokines ; Chemotaxis ; Colon ; Colon cancer ; Colonic diseases ; Colonic Neoplasms - genetics ; Colonic Neoplasms - metabolism ; Colorectal cancer ; Cytokines ; Cytokines - metabolism ; Development and progression ; Embryogenesis ; Embryonic growth stage ; Enzyme-Linked Immunosorbent Assay ; Epithelial cells ; Exposure ; Fluorescent Antibody Technique ; Gene expression ; Genetic aspects ; Hedgehog protein ; Hedgehog Proteins - agonists ; Hedgehog Proteins - genetics ; Hedgehog Proteins - metabolism ; HT29 Cells ; Humans ; Immune response ; Immune system ; Immunofluorescence ; Inflammation ; Interleukin 8 ; Interleukin-8 - metabolism ; Kruppel-Like Transcription Factors - genetics ; Kruppel-Like Transcription Factors - metabolism ; Medicine ; Monocyte chemoattractant protein 1 ; Oncogene Proteins - genetics ; Oncogene Proteins - metabolism ; Physiological aspects ; Proteins ; Pyridines - pharmacology ; Pyrimidines - pharmacology ; Real-Time Polymerase Chain Reaction ; Signal transduction ; Signal Transduction - drug effects ; Signal Transduction - genetics ; Signaling ; Trans-Activators - genetics ; Trans-Activators - metabolism ; Transcription factors ; Veratrum Alkaloids - pharmacology ; Zinc Finger Protein GLI1 ; Zinc Finger Protein Gli2</subject><ispartof>PloS one, 2012-09, Vol.7 (9), p.e45332</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>Yoshimoto 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>2012 Yoshimoto et al 2012 Yoshimoto et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-6d8db6a6fd70b6c4ea8aa31e9142502c9b321f79b5e7c848a78f83a881164ac93</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3446889/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3446889/$$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/23028941$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yoshimoto, Agnes N</creatorcontrib><creatorcontrib>Bernardazzi, Claudio</creatorcontrib><creatorcontrib>Carneiro, Antonio José V</creatorcontrib><creatorcontrib>Elia, Celeste C S</creatorcontrib><creatorcontrib>Martinusso, Cesonia A</creatorcontrib><creatorcontrib>Ventura, Grasiella M</creatorcontrib><creatorcontrib>Castelo-Branco, Morgana T L</creatorcontrib><creatorcontrib>de Souza, Heitor S P</creatorcontrib><title>Hedgehog pathway signaling regulates human colon carcinoma HT-29 epithelial cell line apoptosis and cytokine secretion</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The Hedgehog (Hh) pathway is involved in embryogenesis and physiologic processes including cell survival and proliferation. We used the HT-29 and other human colon carcinoma cell lines to investigate Hh signaling and biological functions in colonic epithelial cells. HT-29 cells were cultured under different conditions and exposed to various stimuli. The expression of Hh pathway components and related genes and proteins were assessed by real-time PCR and immunofluorescence. Viability, apoptosis and cell proliferation were measured by the MTT assay, Annexin-V/7-AAD staining and BrdU uptake, respectively. Chemokines production was measured by ELISA in culture supernatants. Indian and Sonic Hh mRNA levels and the downstream transcription factors Gli-1 and Gli-2 increased following treatment with Hh agonists and butyrate, but decreased upon exposure to cyclopamine or GANT61. BMP4 and BMP7 expression increased after stimulation with Hh agonists. Gli-1 protein expression increased after Hh agonists and decreased following cyclopamine. Exposure to Hh agonists promoted β-catenin reduction and subcellular redistribution. Levels of IL-8 and MCP-1 decreased upon exposure to Hh agonists compared to Hh antagonists, LPS, IFN-γ or EGF. Monocyte chemotaxis decreased upon exposure to supernatants of HT-29 cells treated with Shh compared to Hh antagonists, LPS and IFN-γ. Cellular incorporation of BrdU and cell viability decreased following Hh blockade. Hh agonists abrogated the anti-CD95 induced apoptosis. Hh pathway is a key controller of colon cancer cells, as demonstrated by its effect in dampening inflammatory signals and antagonizing apoptosis. The differential expression of Hh components may underlie abnormalities in the local immune response and in epithelial barrier integrity, with potential homeostatic implications for the development of colonic inflammation and malignancies.</description><subject>Abnormalities</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>beta Catenin - genetics</subject><subject>beta Catenin - metabolism</subject><subject>Biology</subject><subject>Bone Morphogenetic Protein 4 - genetics</subject><subject>Bone Morphogenetic Protein 4 - metabolism</subject><subject>Bone Morphogenetic Protein 7 - genetics</subject><subject>Bone Morphogenetic Protein 7 - metabolism</subject><subject>Breast cancer</subject><subject>Butyrates - pharmacology</subject><subject>CD95 antigen</subject><subject>Cell culture</subject><subject>Cell cycle</subject><subject>Cell proliferation</subject><subject>Cell survival</subject><subject>Cell Survival - drug effects</subject><subject>Cell Survival - genetics</subject><subject>Chemokine CCL2 - genetics</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Chemokines</subject><subject>Chemotaxis</subject><subject>Colon</subject><subject>Colon cancer</subject><subject>Colonic diseases</subject><subject>Colonic Neoplasms - genetics</subject><subject>Colonic Neoplasms - metabolism</subject><subject>Colorectal cancer</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Development and progression</subject><subject>Embryogenesis</subject><subject>Embryonic growth stage</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Epithelial cells</subject><subject>Exposure</subject><subject>Fluorescent Antibody Technique</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Hedgehog protein</subject><subject>Hedgehog Proteins - agonists</subject><subject>Hedgehog Proteins - genetics</subject><subject>Hedgehog Proteins - metabolism</subject><subject>HT29 Cells</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Immunofluorescence</subject><subject>Inflammation</subject><subject>Interleukin 8</subject><subject>Interleukin-8 - metabolism</subject><subject>Kruppel-Like Transcription Factors - genetics</subject><subject>Kruppel-Like Transcription Factors - metabolism</subject><subject>Medicine</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Oncogene Proteins - genetics</subject><subject>Oncogene Proteins - metabolism</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Pyridines - pharmacology</subject><subject>Pyrimidines - pharmacology</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - genetics</subject><subject>Signaling</subject><subject>Trans-Activators - genetics</subject><subject>Trans-Activators - metabolism</subject><subject>Transcription factors</subject><subject>Veratrum Alkaloids - pharmacology</subject><subject>Zinc Finger Protein GLI1</subject><subject>Zinc Finger Protein Gli2</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl-L1DAUxYso7rr6DUQLguDDjPnXNnkRlkWdgYUFXX0Nd9LbNmum6Tbp6nx7M87sMgMKUkjDze-c3FxOlr2kZE55Rd_f-Gnswc0H3-OcEFFwzh5lp1RxNisZ4Y8P9ifZsxBuCCm4LMun2QnjhEkl6Gl2t8C6xc63-QCx-wmbPNg22dq-zUdsJwcRQ95Na-hz451PK4zG9n4N-eJ6xlSOg40dOgsuN-hcnqSYw-CH6IMNOfR1bjbR_9iWA5oRo_X98-xJAy7gi_3_LPv26eP1xWJ2efV5eXF-OTOlYnFW1rJelVA2dUVWpREIEoBTVFSwgjCjVpzRplKrAisjhYRKNpKDlJSWAoziZ9nrne_gfND7kQVNuRBFVSghErHcEbWHGz2Mdg3jRnuw-k_Bj62GMVrjUJeGS2w4I0ooAUSAIgVrioaySiismuT1YX_btFpjbbCPI7gj0-OT3na69Xc6tVNKuW33zd5g9LcThviPlvdUC6kr2zc-mZm1DUafCyVZydLzEzX_C5W-GtfWpNA0NtWPBO-OBImJ-Cu2MIWgl1-__D979f2YfXvAdggudsG7aZuDcAyKHWhGH8KIzcPkKNHbzN9PQ28zr_eZT7JXh1N_EN2HnP8GqJD9BQ</recordid><startdate>20120919</startdate><enddate>20120919</enddate><creator>Yoshimoto, Agnes N</creator><creator>Bernardazzi, Claudio</creator><creator>Carneiro, Antonio José V</creator><creator>Elia, Celeste C S</creator><creator>Martinusso, Cesonia A</creator><creator>Ventura, Grasiella M</creator><creator>Castelo-Branco, Morgana T L</creator><creator>de Souza, Heitor S P</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20120919</creationdate><title>Hedgehog pathway signaling regulates human colon carcinoma HT-29 epithelial cell line apoptosis and cytokine secretion</title><author>Yoshimoto, Agnes N ; Bernardazzi, Claudio ; Carneiro, Antonio José V ; Elia, Celeste C S ; Martinusso, Cesonia A ; Ventura, Grasiella M ; Castelo-Branco, Morgana T L ; de Souza, Heitor S P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-6d8db6a6fd70b6c4ea8aa31e9142502c9b321f79b5e7c848a78f83a881164ac93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Abnormalities</topic><topic>Apoptosis</topic><topic>Apoptosis - 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pharmacology</topic><topic>Pyrimidines - pharmacology</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - genetics</topic><topic>Signaling</topic><topic>Trans-Activators - genetics</topic><topic>Trans-Activators - metabolism</topic><topic>Transcription factors</topic><topic>Veratrum Alkaloids - pharmacology</topic><topic>Zinc Finger Protein GLI1</topic><topic>Zinc Finger Protein Gli2</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yoshimoto, Agnes N</creatorcontrib><creatorcontrib>Bernardazzi, Claudio</creatorcontrib><creatorcontrib>Carneiro, Antonio José V</creatorcontrib><creatorcontrib>Elia, Celeste C S</creatorcontrib><creatorcontrib>Martinusso, Cesonia A</creatorcontrib><creatorcontrib>Ventura, Grasiella M</creatorcontrib><creatorcontrib>Castelo-Branco, Morgana T L</creatorcontrib><creatorcontrib>de Souza, Heitor S P</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</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>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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We used the HT-29 and other human colon carcinoma cell lines to investigate Hh signaling and biological functions in colonic epithelial cells. HT-29 cells were cultured under different conditions and exposed to various stimuli. The expression of Hh pathway components and related genes and proteins were assessed by real-time PCR and immunofluorescence. Viability, apoptosis and cell proliferation were measured by the MTT assay, Annexin-V/7-AAD staining and BrdU uptake, respectively. Chemokines production was measured by ELISA in culture supernatants. Indian and Sonic Hh mRNA levels and the downstream transcription factors Gli-1 and Gli-2 increased following treatment with Hh agonists and butyrate, but decreased upon exposure to cyclopamine or GANT61. BMP4 and BMP7 expression increased after stimulation with Hh agonists. Gli-1 protein expression increased after Hh agonists and decreased following cyclopamine. Exposure to Hh agonists promoted β-catenin reduction and subcellular redistribution. Levels of IL-8 and MCP-1 decreased upon exposure to Hh agonists compared to Hh antagonists, LPS, IFN-γ or EGF. Monocyte chemotaxis decreased upon exposure to supernatants of HT-29 cells treated with Shh compared to Hh antagonists, LPS and IFN-γ. Cellular incorporation of BrdU and cell viability decreased following Hh blockade. Hh agonists abrogated the anti-CD95 induced apoptosis. Hh pathway is a key controller of colon cancer cells, as demonstrated by its effect in dampening inflammatory signals and antagonizing apoptosis. The differential expression of Hh components may underlie abnormalities in the local immune response and in epithelial barrier integrity, with potential homeostatic implications for the development of colonic inflammation and malignancies.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23028941</pmid><doi>10.1371/journal.pone.0045332</doi><tpages>e45332</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2012-09, Vol.7 (9), p.e45332 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1344575944 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Abnormalities Apoptosis Apoptosis - drug effects Apoptosis - genetics beta Catenin - genetics beta Catenin - metabolism Biology Bone Morphogenetic Protein 4 - genetics Bone Morphogenetic Protein 4 - metabolism Bone Morphogenetic Protein 7 - genetics Bone Morphogenetic Protein 7 - metabolism Breast cancer Butyrates - pharmacology CD95 antigen Cell culture Cell cycle Cell proliferation Cell survival Cell Survival - drug effects Cell Survival - genetics Chemokine CCL2 - genetics Chemokine CCL2 - metabolism Chemokines Chemotaxis Colon Colon cancer Colonic diseases Colonic Neoplasms - genetics Colonic Neoplasms - metabolism Colorectal cancer Cytokines Cytokines - metabolism Development and progression Embryogenesis Embryonic growth stage Enzyme-Linked Immunosorbent Assay Epithelial cells Exposure Fluorescent Antibody Technique Gene expression Genetic aspects Hedgehog protein Hedgehog Proteins - agonists Hedgehog Proteins - genetics Hedgehog Proteins - metabolism HT29 Cells Humans Immune response Immune system Immunofluorescence Inflammation Interleukin 8 Interleukin-8 - metabolism Kruppel-Like Transcription Factors - genetics Kruppel-Like Transcription Factors - metabolism Medicine Monocyte chemoattractant protein 1 Oncogene Proteins - genetics Oncogene Proteins - metabolism Physiological aspects Proteins Pyridines - pharmacology Pyrimidines - pharmacology Real-Time Polymerase Chain Reaction Signal transduction Signal Transduction - drug effects Signal Transduction - genetics Signaling Trans-Activators - genetics Trans-Activators - metabolism Transcription factors Veratrum Alkaloids - pharmacology Zinc Finger Protein GLI1 Zinc Finger Protein Gli2 |
| title | Hedgehog pathway signaling regulates human colon carcinoma HT-29 epithelial cell line apoptosis and cytokine secretion |
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