GUCY2C Opposes Systemic Genotoxic Tumorigenesis by Regulating AKT-Dependent Intestinal Barrier Integrity
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{"title"=>"GUCY2C opposes systemic genotoxic tumorigenesis by regulating AKT-dependent intestinal barrier integrity", "type"=>"journal", "authors"=>[{"first_name"=>"Jieru Egeria", "last_name"=>"Lin", "scopus_author_id"=>"23467242500"}, {"first_name"=>"Adam Eugene", "last_name"=>"Snook", "scopus_author_id"=>"21741293800"}, {"first_name"=>"Peng", "last_name"=>"Li", "scopus_author_id"=>"57191265166"}, {"first_name"=>"Brian Arthur", "last_name"=>"Stoecker", "scopus_author_id"=>"36998802100"}, {"first_name"=>"Gilbert Won", "last_name"=>"Kim", "scopus_author_id"=>"23992630100"}, {"first_name"=>"Michael Sullivan", "last_name"=>"Magee", "scopus_author_id"=>"56727822000"}, {"first_name"=>"Alex Vladimir Mejia", "last_name"=>"Garcia", "scopus_author_id"=>"55271656100"}, {"first_name"=>"Michael Anthony", "last_name"=>"Valentino", "scopus_author_id"=>"35244081700"}, {"first_name"=>"Terry", "last_name"=>"Hyslop", "scopus_author_id"=>"6701898718"}, {"first_name"=>"Stephanie", "last_name"=>"Schulz", "scopus_author_id"=>"7201851192"}, {"first_name"=>"Scott Arthur", "last_name"=>"Waldman", "scopus_author_id"=>"7102179927"}], "year"=>2012, "source"=>"PLoS ONE", "identifiers"=>{"scopus"=>"2-s2.0-84863180511", "sgr"=>"84863180511", "issn"=>"19326203", "isbn"=>"1932-6203 (Electronic)\\r1932-6203 (Linking)", "pmid"=>"22384056", "doi"=>"10.1371/journal.pone.0031686", "pui"=>"364330087"}, "id"=>"935eff45-5fb9-3a68-a67e-167d101a18ac", "abstract"=>"The barrier separating mucosal and systemic compartments comprises epithelial cells, annealed by tight junctions, limiting permeability. GUCY2C recently emerged as an intestinal tumor suppressor coordinating AKT1-dependent crypt-villus homeostasis. Here, the contribution of GUCY2C to barrier integrity opposing colitis and systemic tumorigenesis is defined. Mice deficient in GUCY2C (Gucy2c(-/-)) exhibited barrier hyperpermeability associated with reduced junctional proteins. Conversely, activation of GUCY2C in mice reduced barrier permeability associated with increased junctional proteins. Further, silencing GUCY2C exacerbated, while activation reduced, chemical barrier disruption and colitis. Moreover, eliminating GUCY2C amplified, while activation reduced, systemic oxidative DNA damage. This genotoxicity was associated with increased spontaneous and carcinogen-induced systemic tumorigenesis in Gucy2c(-/-) mice. GUCY2C regulated barrier integrity by repressing AKT1, associated with increased junction proteins occludin and claudin 4 in mice and Caco2 cells in vitro. Thus, GUCY2C defends the intestinal barrier, opposing colitis and systemic genotoxicity and tumorigenesis. The therapeutic potential of this observation is underscored by the emerging clinical development of oral GUCY2C ligands, which can be used for chemoprophylaxis in inflammatory bowel disease and cancer.", "link"=>"http://www.mendeley.com/research/gucy2c-opposes-systemic-genotoxic-tumorigenesis-regulating-aktdependent-intestinal-barrier-integrity", "reader_count"=>26, "reader_count_by_academic_status"=>{"Unspecified"=>2, "Professor > Associate Professor"=>1, "Researcher"=>8, "Student > Ph. D. Student"=>7, "Student > Postgraduate"=>2, "Other"=>2, "Student > Master"=>2, "Student > Bachelor"=>1, "Professor"=>1}, "reader_count_by_user_role"=>{"Unspecified"=>2, "Professor > Associate Professor"=>1, "Researcher"=>8, "Student > Ph. D. Student"=>7, "Student > Postgraduate"=>2, "Other"=>2, "Student > Master"=>2, "Student > Bachelor"=>1, "Professor"=>1}, "reader_count_by_subject_area"=>{"Unspecified"=>2, "Environmental Science"=>1, "Biochemistry, Genetics and Molecular Biology"=>3, "Agricultural and Biological Sciences"=>9, "Medicine and Dentistry"=>7, "Pharmacology, Toxicology and Pharmaceutical Science"=>1, "Physics and Astronomy"=>2, "Immunology and Microbiology"=>1}, "reader_count_by_subdiscipline"=>{"Medicine and Dentistry"=>{"Medicine and Dentistry"=>7}, "Physics and Astronomy"=>{"Physics and Astronomy"=>2}, "Immunology and Microbiology"=>{"Immunology and Microbiology"=>1}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>9}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>3}, "Unspecified"=>{"Unspecified"=>2}, "Environmental Science"=>{"Environmental Science"=>1}, "Pharmacology, Toxicology and Pharmaceutical Science"=>{"Pharmacology, Toxicology and Pharmaceutical Science"=>1}}, "reader_count_by_country"=>{"United States"=>1, "India"=>1}, "group_count"=>0}

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Figshare

  • {"files"=>["https://ndownloader.figshare.com/files/677357"], "description"=>"<p>(<b>A</b>) Comparison of mRNA expression of genes associated with the canonical tight junction pathway (KEGG 04530) of <i>Gucy2c<sup>+/+</sup></i> and <i>Gucy2c<sup>−/−</sup></i> mice (n = 4, p = 0.029). (<b>B</b>) Immunoblot analysis of tight junction proteins from the distal colon of 12 week old <i>Gucy2c<sup>+/+</sup></i> and <i>Gucy2c<sup>−/−</sup></i> mice. Data represent means of n≥7±SEM. (<b>C</b>) Immunofluorescence staining of claudin 4 from the distal colon of 12 week old <i>Gucy2c<sup>+/+</sup></i> and <i>Gucy2c<sup>−/−</sup></i> mice. (Nucleus-DAPI, β-catenin-red, Claudin 4-green; 1,000×). (<b>D</b>) Transmission electron microscopy of tight junction complexes from jejuna of 12 week old <i>Gucy2c<sup>+/+</sup></i> and <i>Gucy2c<sup>−/−</sup></i> mice (25,000×). (<b>E</b>) FITC-dextran was administered by oral gavage to age-matched <i>Gucy2c<sup>+/+</sup></i> and <i>Gucy2c<sup>−/−</sup></i> mice after an overnight fast. Serum fluorescence was analyzed 90 min after gavage. One representative experiment of three (n = 3). *, p<0.05, **, p<0.01.</p>", "links"=>[], "tags"=>["regulates", "intestinal"], "article_id"=>347838, "categories"=>["Cancer", "Molecular Biology", "Chemistry"], "users"=>["Jieru Egeria Lin", "Adam Eugene Snook", "Peng Li", "Brian Arthur Stoecker", "Gilbert Won Kim", "Michael Sullivan Magee", "Alex Vladimir Mejia Garcia", "Michael Anthony Valentino", "Terry Hyslop", "Stephanie Schulz", "Scott Arthur Waldman"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0031686.g001", "stats"=>{"downloads"=>0, "page_views"=>1, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_GUCY2C_regulates_intestinal_barrier_integrity_/347838", "title"=>"GUCY2C regulates intestinal barrier integrity.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-02-22 02:10:38"}
  • {"files"=>["https://ndownloader.figshare.com/files/678295"], "description"=>"<p>(<b>A</b>) Immunoblot analysis of tight junction proteins from jejuna of 12 week-old mice (n≥7). Data represent means ± SEM. Blue asterisks compare results to <i>Gucy2c<sup>+/+</sup></i>, black asterisks compare results to <i>Gucy2c<sup>−/</sup></i>. (<b>B</b>) Intestinal permeability was examined by serum fluorescence 90 min after FITC-dextran gavage. Each point represents one mouse. (<b>C</b>) Regulation of AKT phosphorylation by GUCY2C signaling in Caco2 human colon cancer cells was examined by immunoblot analysis. Data represent means ± SEM of 3 experiments done in duplicate. (<b>D</b>) AKT1 signaling in Caco2 cells was manipulated by adenovirus-delivered AKT1 (WTAKT1), constitutive active AKT1 mutant (MyrAKT1), or siRNA against AKT1 (siAKT1). Two days after infection, cells were treated with ST for 6 d. Barrier permeability was examined by FITC-dextran diffusion. Data represent mean ± SEM obtained from one of five experiments done in triplicate. (<b>E</b>) Tight junction protein expression was examined by immunoblot analysis in Caco2 cells stably expressing empty vector (MSCV) or shRNA against AKT1 (shAKT1) after 6 d of ST treatment. Data represent means ± SEM of three experiments done in duplicate. Blue asterisks compare results to MSCV-PBS, black asterisks compare results to MSCV-ST. *, p<0.05, **, p<0.01, ***, p<0.001. In C–E, statistical analyses were compared to PBS control.</p>", "links"=>[], "tags"=>["molecular biology", "oncology", "Gastroenterology and hepatology"], "article_id"=>348774, "categories"=>["Cancer", "Molecular Biology", "Chemistry"], "users"=>["Jieru Egeria Lin", "Adam Eugene Snook", "Peng Li", "Brian Arthur Stoecker", "Gilbert Won Kim", "Michael Sullivan Magee", "Alex Vladimir Mejia Garcia", "Michael Anthony Valentino", "Terry Hyslop", "Stephanie Schulz", "Scott Arthur Waldman"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0031686.g006", "stats"=>{"downloads"=>0, "page_views"=>6, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_GUCY2C_regulation_of_barrier_integrity_is_AKT1_dependent_/348774", "title"=>"GUCY2C regulation of barrier integrity is AKT1-dependent.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-02-22 02:26:14"}
  • {"files"=>["https://ndownloader.figshare.com/files/677558"], "description"=>"<p><i>Gucy2c<sup>+/+</sup></i> and <i>Gucy2c<sup>−/−</sup></i> male mice were administered 3% DSS in drinking water for 7 d to disrupt the epithelial barrier and induce colitis. Severity of colitis was analyzed by (<b>A</b>) body weight (n = 11) and (<b>B</b>) survival (n≥11). (<b>C</b>) Colon length was measured from the colocecal junction to the anal verge on day 12 (5 d post-DSS exposure) to quantify chronic inflammation. (<b>D</b>) Histological sections obtained from jejunum and distal colon on day 12 were stained with H&E and scored for epithelial and mesenchymal inflammation. Each point represents one mouse. (<b>E</b>) Representative H&E colon sections (20×). Data are mean ± SD (in C) and SEM (in D) obtained from one of three independent experiments. **, p<0.01, ***, p<0.001.</p>", "links"=>[], "tags"=>["increases", "susceptibility", "dss-induced"], "article_id"=>348035, "categories"=>["Cancer", "Molecular Biology", "Chemistry"], "users"=>["Jieru Egeria Lin", "Adam Eugene Snook", "Peng Li", "Brian Arthur Stoecker", "Gilbert Won Kim", "Michael Sullivan Magee", "Alex Vladimir Mejia Garcia", "Michael Anthony Valentino", "Terry Hyslop", "Stephanie Schulz", "Scott Arthur Waldman"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0031686.g002", "stats"=>{"downloads"=>1, "page_views"=>9, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_GUCY2C_deficiency_increases_susceptibility_to_DSS_induced_colitis_/348035", "title"=>"GUCY2C-deficiency increases susceptibility to DSS-induced colitis.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-02-22 02:13:55"}
  • {"files"=>["https://ndownloader.figshare.com/files/677735"], "description"=>"<p>Constitutive expression of GUCA2A was initiated by Cre recombinase expressed in intestinal epithelial cells after 5 days of IP tamoxifen administration in <i>ROSA-Guca2a</i>×<i>Vil-Cre/ER<sup>T2</sup></i> male mice. Two days later, 3% DSS was administrated for 7 d to induce colitis. (<b>A</b>) Intestinal macromolecular permeability was assessed on day 10 (3 d post-DSS exposure) by serum fluorescence 90 min after FITC-dextran gavage (n≥5). Severity of colitis was quantified by (<b>B</b>) body weight and (<b>C</b>) survival (n≥15). Data represent one of three independent experiments. Inflammation was quantified by (<b>D</b>) colon length and (<b>E</b>) histological score on day 10 (n≥5). Each point represents one mouse. (<b>F</b>) Representative H&E colon sections (20×). Data are mean ± SEM. *, p<0.05.</p>", "links"=>[], "tags"=>["guca2a", "intestine", "suppresses", "dss-induced"], "article_id"=>348212, "categories"=>["Cancer", "Molecular Biology", "Chemistry"], "users"=>["Jieru Egeria Lin", "Adam Eugene Snook", "Peng Li", "Brian Arthur Stoecker", "Gilbert Won Kim", "Michael Sullivan Magee", "Alex Vladimir Mejia Garcia", "Michael Anthony Valentino", "Terry Hyslop", "Stephanie Schulz", "Scott Arthur Waldman"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0031686.g003", "stats"=>{"downloads"=>1, "page_views"=>11, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Constitutive_GUCA2A_expression_in_intestine_suppresses_DSS_induced_colitis_/348212", "title"=>"Constitutive GUCA2A expression in intestine suppresses DSS-induced colitis.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-02-22 02:16:52"}
  • {"files"=>["https://ndownloader.figshare.com/files/345889", "https://ndownloader.figshare.com/files/346033", "https://ndownloader.figshare.com/files/346167", "https://ndownloader.figshare.com/files/346301"], "description"=>"<div><p>The barrier separating mucosal and systemic compartments comprises epithelial cells, annealed by tight junctions, limiting permeability. GUCY2C recently emerged as an intestinal tumor suppressor coordinating AKT1-dependent crypt-villus homeostasis. Here, the contribution of GUCY2C to barrier integrity opposing colitis and systemic tumorigenesis is defined. Mice deficient in GUCY2C (<em>Gucy2c<sup>−/−</sup></em>) exhibited barrier hyperpermeability associated with reduced junctional proteins. Conversely, activation of GUCY2C in mice reduced barrier permeability associated with increased junctional proteins. Further, silencing GUCY2C exacerbated, while activation reduced, chemical barrier disruption and colitis. Moreover, eliminating GUCY2C amplified, while activation reduced, systemic oxidative DNA damage. This genotoxicity was associated with increased spontaneous and carcinogen-induced systemic tumorigenesis in <em>Gucy2c<sup>−/−</sup></em> mice. GUCY2C regulated barrier integrity by repressing AKT1, associated with increased junction proteins occludin and claudin 4 in mice and Caco2 cells in vitro. Thus, GUCY2C defends the intestinal barrier, opposing colitis and systemic genotoxicity and tumorigenesis. The therapeutic potential of this observation is underscored by the emerging clinical development of oral GUCY2C ligands, which can be used for chemoprophylaxis in inflammatory bowel disease and cancer.</p> </div>", "links"=>[], "tags"=>["gucy2c", "opposes", "systemic", "genotoxic", "tumorigenesis", "regulating", "akt-dependent", "intestinal"], "article_id"=>128362, "categories"=>["Cancer", "Molecular Biology", "Chemistry"], "users"=>["Jieru Egeria Lin", "Adam Eugene Snook", "Peng Li", "Brian Arthur Stoecker", "Gilbert Won Kim", "Michael Sullivan Magee", "Alex Vladimir Mejia Garcia", "Michael Anthony Valentino", "Terry Hyslop", "Stephanie Schulz", "Scott Arthur Waldman"], "doi"=>["https://dx.doi.org/10.1371/journal.pone.0031686.s001", "https://dx.doi.org/10.1371/journal.pone.0031686.s002", "https://dx.doi.org/10.1371/journal.pone.0031686.s003", "https://dx.doi.org/10.1371/journal.pone.0031686.s004"], "stats"=>{"downloads"=>5, "page_views"=>6, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/GUCY2C_Opposes_Systemic_Genotoxic_Tumorigenesis_by_Regulating_AKT_Dependent_Intestinal_Barrier_Integrity/128362", "title"=>"GUCY2C Opposes Systemic Genotoxic Tumorigenesis by Regulating AKT-Dependent Intestinal Barrier Integrity", "pos_in_sequence"=>0, "defined_type"=>4, "published_date"=>"2012-02-22 02:19:22"}
  • {"files"=>["https://ndownloader.figshare.com/files/678147"], "description"=>"<p>(<b>A</b>) Eliminating GUCY2C increases basal DNA oxidation in leukocytes. Each point represents one mouse. (<b>B</b>) Oral ST supplementation decreases DSS-induced hepatic genotoxicity. <i>Gucy2c<sup>+/+</sup></i> mice were preconditioned with oral ST for 6 d, and then treated with 3.5% DSS for 7 d, followed by quantification of DNA oxidation in liver on days 10 (n≥5) and 13 (n≥2; 3 and 6 d post-DSS exposure). Data represent mean ± SD. (<b>C</b>) <i>Gucy2c<sup>−/−</sup></i> mice exhibited a higher incidence of spontaneous tumors comparing with age-matched 2-year-old <i>Gucy2c<sup>+/+</sup></i> mice (n≥14, p = 0.02). (<b>D</b>) The carcinogen AOM induced hepatoma in <i>Gucy2c<sup>−/−</sup></i>, but not <i>Gucy2c<sup>+/+</sup></i>, mice (n≥10, p = 0.04). C and D are analyzed by two-sided Fisher's exact test. *, p<0.05.</p>", "links"=>[], "tags"=>["modulates", "systemic", "genotoxicity"], "article_id"=>348630, "categories"=>["Cancer", "Molecular Biology", "Chemistry"], "users"=>["Jieru Egeria Lin", "Adam Eugene Snook", "Peng Li", "Brian Arthur Stoecker", "Gilbert Won Kim", "Michael Sullivan Magee", "Alex Vladimir Mejia Garcia", "Michael Anthony Valentino", "Terry Hyslop", "Stephanie Schulz", "Scott Arthur Waldman"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0031686.g005", "stats"=>{"downloads"=>1, "page_views"=>5, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_GUCY2C_modulates_systemic_genotoxicity_and_tumorigenesis_/348630", "title"=>"GUCY2C modulates systemic genotoxicity and tumorigenesis.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-02-22 02:23:50"}
  • {"files"=>["https://ndownloader.figshare.com/files/677971"], "description"=>"<p>C57B6 female mice were administered control peptide (CP) or ST to examine the effect of GUCY2C activation on intestinal permeability after 14 d of oral ligand supplementation. (<b>A</b>) Serum fluorescence was analyzed 90 min after FITC-dextran gavage (n = 21) following 6 d of ligand supplementation. (<b>B, C</b>) Following 14 d of ST pre-conditioning, 3.5% DSS was administrated for 7 d to induce colitis which was quantified by (<b>B</b>) body weight and (<b>C</b>) survival. Data represent one of two independent experiments. Severity of colitis was quantified by (<b>D</b>) colon length, measured on day 10 (3 d post-DSS exposure), and gross anatomic analysis of colons from ST-, compared to CP-, preconditioned mice demonstrated normal stool formation (n = 21) and (<b>E</b>) histological score on day 10. Each point represents one mouse. (<b>F</b>) Representative H&E colon sections (20×). *, p<0.05, **, p<0.01.</p>", "links"=>[], "tags"=>["ligand", "supplementation", "decreases", "intestinal", "permeability", "susceptibility", "dss-induced"], "article_id"=>348447, "categories"=>["Cancer", "Molecular Biology", "Chemistry"], "users"=>["Jieru Egeria Lin", "Adam Eugene Snook", "Peng Li", "Brian Arthur Stoecker", "Gilbert Won Kim", "Michael Sullivan Magee", "Alex Vladimir Mejia Garcia", "Michael Anthony Valentino", "Terry Hyslop", "Stephanie Schulz", "Scott Arthur Waldman"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0031686.g004", "stats"=>{"downloads"=>0, "page_views"=>9, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_GUCY2C_ligand_supplementation_decreases_intestinal_permeability_and_susceptibility_to_DSS_induced_colitis_/348447", "title"=>"GUCY2C ligand supplementation decreases intestinal permeability and susceptibility to DSS-induced colitis.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-02-22 02:20:47"}

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