id paper:paper_19492553_v8_n3_p4690_Sapochnik
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spelling paper:paper_19492553_v8_n3_p4690_Sapochnik2023-06-08T16:32:40Z Autocrine IL-6 mediates pituitary tumor senescence Haedo, Mariana Raquel Autocrine Benign tumor IL-6 Pituitary tumor Senescence beta galactosidase cyclin dependent kinase inhibitor 2A growth hormone interleukin 6 senescence associated beta galactosidase short hairpin RNA tumor marker unclassified drug animal experiment animal model animal tissue Article autocrine effect carcinogenicity cell aging cell culture cell invasion cell proliferation controlled study enzyme activity enzyme analysis gene expression gene silencing human human cell human tissue hypophysis adenoma hypophysis tumor in vitro study in vivo study interferon production male molecular cloning mouse nonhuman pathogenesis phenotype protein expression senescence wild type Cellular senescence is a stable proliferative arrest state. Pituitary adenomas are frequent and mostly benign, but the mechanism for this remains unknown. IL-6 is involved in pituitary tumor progression and is produced by the tumoral cells. In a cell autonomous fashion, IL-6 participates in oncogene-induced senescence in transduced human melanocytes. Here we prove that autocrine IL-6 participates in pituitary tumor senescence. Endogenous IL-6 inhibition in somatotroph MtT/S shRNA stable clones results in decreased SA-β-gal activity and p16INK4a but increased pRb, proliferation and invasion. Nude mice injected with IL-6 silenced clones develop tumors contrary to MtT/S wild type that do not, demonstrating that clones that escape senescence are capable of becoming tumorigenic. When endogenous IL-6 is silenced, cell cultures derived from positive SA-β-gal human tumor samples decrease the expression of the senescence marker. Our results establish that IL-6 contributes to maintain senescence by its autocrine action, providing a natural model of IL-6 mediated benign adenoma senescence. Fil:Haedo, M.R. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2017 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_19492553_v8_n3_p4690_Sapochnik http://hdl.handle.net/20.500.12110/paper_19492553_v8_n3_p4690_Sapochnik
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic Autocrine
Benign tumor
IL-6
Pituitary tumor
Senescence
beta galactosidase
cyclin dependent kinase inhibitor 2A
growth hormone
interleukin 6
senescence associated beta galactosidase
short hairpin RNA
tumor marker
unclassified drug
animal experiment
animal model
animal tissue
Article
autocrine effect
carcinogenicity
cell aging
cell culture
cell invasion
cell proliferation
controlled study
enzyme activity
enzyme analysis
gene expression
gene silencing
human
human cell
human tissue
hypophysis adenoma
hypophysis tumor
in vitro study
in vivo study
interferon production
male
molecular cloning
mouse
nonhuman
pathogenesis
phenotype
protein expression
senescence
wild type
spellingShingle Autocrine
Benign tumor
IL-6
Pituitary tumor
Senescence
beta galactosidase
cyclin dependent kinase inhibitor 2A
growth hormone
interleukin 6
senescence associated beta galactosidase
short hairpin RNA
tumor marker
unclassified drug
animal experiment
animal model
animal tissue
Article
autocrine effect
carcinogenicity
cell aging
cell culture
cell invasion
cell proliferation
controlled study
enzyme activity
enzyme analysis
gene expression
gene silencing
human
human cell
human tissue
hypophysis adenoma
hypophysis tumor
in vitro study
in vivo study
interferon production
male
molecular cloning
mouse
nonhuman
pathogenesis
phenotype
protein expression
senescence
wild type
Haedo, Mariana Raquel
Autocrine IL-6 mediates pituitary tumor senescence
topic_facet Autocrine
Benign tumor
IL-6
Pituitary tumor
Senescence
beta galactosidase
cyclin dependent kinase inhibitor 2A
growth hormone
interleukin 6
senescence associated beta galactosidase
short hairpin RNA
tumor marker
unclassified drug
animal experiment
animal model
animal tissue
Article
autocrine effect
carcinogenicity
cell aging
cell culture
cell invasion
cell proliferation
controlled study
enzyme activity
enzyme analysis
gene expression
gene silencing
human
human cell
human tissue
hypophysis adenoma
hypophysis tumor
in vitro study
in vivo study
interferon production
male
molecular cloning
mouse
nonhuman
pathogenesis
phenotype
protein expression
senescence
wild type
description Cellular senescence is a stable proliferative arrest state. Pituitary adenomas are frequent and mostly benign, but the mechanism for this remains unknown. IL-6 is involved in pituitary tumor progression and is produced by the tumoral cells. In a cell autonomous fashion, IL-6 participates in oncogene-induced senescence in transduced human melanocytes. Here we prove that autocrine IL-6 participates in pituitary tumor senescence. Endogenous IL-6 inhibition in somatotroph MtT/S shRNA stable clones results in decreased SA-β-gal activity and p16INK4a but increased pRb, proliferation and invasion. Nude mice injected with IL-6 silenced clones develop tumors contrary to MtT/S wild type that do not, demonstrating that clones that escape senescence are capable of becoming tumorigenic. When endogenous IL-6 is silenced, cell cultures derived from positive SA-β-gal human tumor samples decrease the expression of the senescence marker. Our results establish that IL-6 contributes to maintain senescence by its autocrine action, providing a natural model of IL-6 mediated benign adenoma senescence.
author Haedo, Mariana Raquel
author_facet Haedo, Mariana Raquel
author_sort Haedo, Mariana Raquel
title Autocrine IL-6 mediates pituitary tumor senescence
title_short Autocrine IL-6 mediates pituitary tumor senescence
title_full Autocrine IL-6 mediates pituitary tumor senescence
title_fullStr Autocrine IL-6 mediates pituitary tumor senescence
title_full_unstemmed Autocrine IL-6 mediates pituitary tumor senescence
title_sort autocrine il-6 mediates pituitary tumor senescence
publishDate 2017
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_19492553_v8_n3_p4690_Sapochnik
http://hdl.handle.net/20.500.12110/paper_19492553_v8_n3_p4690_Sapochnik
work_keys_str_mv AT haedomarianaraquel autocrineil6mediatespituitarytumorsenescence
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