Autocrine IL-6 mediates pituitary tumor senescence
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...
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Acceso en línea: | 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 |
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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 |
_version_ |
1768543204376838144 |