Literature DB >> 26695862

The Cables1 Gene in Glucocorticoid Regulation of Pituitary Corticotrope Growth and Cushing Disease.

Audrey Roussel-Gervais1, Catherine Couture1, David Langlais1, Shinobu Takayasu1, Aurelio Balsalobre1, Bo R Rueda1, Lawrence R Zukerberg1, Dominique Figarella-Branger1, Thierry Brue1, Jacques Drouin1.   

Abstract

CONTEXT: Cushing disease (CD) is due to pituitary corticotrope adenomas that produce unrestrained ACTH secretion and have lost the negative feedback exerted by glucocorticoids (GCs). GCs also restrain corticotrope proliferation, and the mechanisms of this inhibition are poorly understood.
OBJECTIVE: The aim of the study was to identify cell cycle regulatory genes that are regulated by GCs and the glucocorticoid receptor and to assess regulatory genes that have a rate-limiting action on corticotrope proliferation and may be disregulated in CD.
DESIGN: The mouse corticotrope tumor cells AtT-20 were used to identify GC-regulated genes that contribute to control of cell cycle progression. Surgery sections from patients with CD were used to assess expression of CABLES1 in corticotrope adenomas.
METHODS: Gene expression profiling, small interfering RNA knockdowns, cell cycle analyses, and genetic manipulations were performed in AtT-20 cells. Sequencing of chromatin immunoprecipitation for pituitary-restricted transcription factors and RNA polymerase II were used to identify regulatory elements and genes that bind GR and are direct transcriptional targets. A panel of previously well-characterized corticotrope adenomas was used to correlate expression of CABLES1 with that of other markers.
RESULTS: GCs altered expression of 3 positive and 3 negative regulators of cell cycle progression. Two Myc genes (L-Myc and N-Myc) and E2F2 are repressed by GCs, whereas genes for the negative regulators of the cell cycle, Gadd45β, Gadd45γ, and Cables1 are activated by GCs. Cables1 small interfering RNA knockdown strongly stimulates AtT-20 cell proliferation and antagonizes the growth inhibition produced by GCs. The Gadd45 and Cables1 genes have the hallmarks of direct GC targets. CABLES1 is expressed in normal human pituitary cells, but expression is lost in ∼55% of corticotrope adenomas, and this is strongly correlated with the loss of p27(Kip1) expression.
CONCLUSIONS: CABLES1 is a critical regulator of corticotrope proliferation that defines a pathway often inactivated in CD and links proliferation to GC resistance.

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Year:  2015        PMID: 26695862     DOI: 10.1210/jc.2015-3324

Source DB:  PubMed          Journal:  J Clin Endocrinol Metab        ISSN: 0021-972X            Impact factor:   5.958


  17 in total

Review 1.  Genetic Basis of ACTH-Secreting Adenomas.

Authors:  Pietro Locantore; Rosa Maria Paragliola; Gianluca Cera; Roberto Novizio; Ettore Maggio; Vittoria Ramunno; Andrea Corsello; Salvatore Maria Corsello
Journal:  Int J Mol Sci       Date:  2022-06-19       Impact factor: 6.208

Review 2.  Molecular Derangements and the Diagnosis of ACTH-Dependent Cushing's Syndrome.

Authors:  Lynnette K Nieman
Journal:  Endocr Rev       Date:  2022-09-26       Impact factor: 25.261

Review 3.  Genetics of Cushing's Syndrome.

Authors:  Laura C Hernández-Ramírez; Constantine A Stratakis
Journal:  Endocrinol Metab Clin North Am       Date:  2018-06       Impact factor: 4.741

4.  A Novel Expression Profile of Cell Cycle and DNA Repair Proteins in Nonfunctioning Pituitary Adenomas.

Authors:  Derya Metin-Armagan; Nil Comunoglu; Gulay Bulut; Pinar Kadioglu; Hiraku Kameda; Nurperi Gazioglu; Necmettin Tanriover; Melek Ozturk
Journal:  Endocr Pathol       Date:  2020-03       Impact factor: 3.943

Review 5.  Recent Understanding and Future Directions of Recurrent Corticotroph Tumors.

Authors:  José Miguel Hinojosa-Amaya; César Ernesto Lam-Chung; Daniel Cuevas-Ramos
Journal:  Front Endocrinol (Lausanne)       Date:  2021-04-26       Impact factor: 5.555

Review 6.  The Molecular Pathology of Cushing Disease: Are We Nearly There?

Authors:  Ashley B Grossman
Journal:  J Endocr Soc       Date:  2017-02-01

7.  Loss-of-function mutations in the CABLES1 gene are a novel cause of Cushing's disease.

Authors:  Laura C Hernández-Ramírez; Ryhem Gam; Nuria Valdés; Maya B Lodish; Nathan Pankratz; Aurelio Balsalobre; Yves Gauthier; Fabio R Faucz; Giampaolo Trivellin; Prashant Chittiboina; John Lane; Denise M Kay; Aggeliki Dimopoulos; Stephan Gaillard; Mario Neou; Jérôme Bertherat; Guillaume Assié; Chiara Villa; James L Mills; Jacques Drouin; Constantine A Stratakis
Journal:  Endocr Relat Cancer       Date:  2017-05-22       Impact factor: 5.678

Review 8.  Aggressive Cushing's Disease: Molecular Pathology and Its Therapeutic Approach.

Authors:  Masaaki Yamamoto; Takahiro Nakao; Wataru Ogawa; Hidenori Fukuoka
Journal:  Front Endocrinol (Lausanne)       Date:  2021-06-16       Impact factor: 5.555

9.  Proopiomelanocortin, glucocorticoid, and CRH receptor expression in human ACTH-secreting pituitary adenomas.

Authors:  Maria Francesca Cassarino; Antonella Sesta; Luca Pagliardini; Marco Losa; Giovanni Lasio; Francesco Cavagnini; Francesca Pecori Giraldi
Journal:  Endocrine       Date:  2016-05-24       Impact factor: 3.633

10.  Impact of energy restriction during late gestation on the muscle and blood transcriptome of beef calves after preconditioning.

Authors:  Leticia P Sanglard; Moysés Nascimento; Philipe Moriel; Jeffrey Sommer; Melissa Ashwell; Matthew H Poore; Márcio de S Duarte; Nick V L Serão
Journal:  BMC Genomics       Date:  2018-09-25       Impact factor: 3.969

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