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Menin inactivation leads to loss of transforming growth factor beta inhibition of parathyroid cell proliferation and parathyroid hormone secretion.
Cancer Res. 2004 Mar 15; 64(6):2222-8.CR

Abstract

Primary hyperparathyroidism is a common endocrine disorder caused by parathyroid gland enlargement and excessive parathyroid hormone (PTH) secretion. However, the precise mechanisms of tumorigenesis of the parathyroids are unknown. Here we have investigated the roles of transforming growth factor (TGF)-beta and menin, the product of the multiple endocrine neoplasia type 1 (Men1) gene, in the proliferation and PTH production of parathyroid cells from either patients with secondary hyperparathyroidism or Men1. TGF-beta was expressed in the parathyroid endocrine cells. Addition of TGF-beta to parathyroid cells from patients with secondary hyperparathyroidism inhibited their proliferation and PTH secretion. These responses to TGF-beta were lost when menin was specifically inactivated by antisense oligonucleotides. Moreover, TGF-beta did not affect the proliferation and PTH production of parathyroid cells from a Men1 patient. These results indicate that menin is required for TGF-beta action in the parathyroid. We conclude that TGF-beta is an important autocrine/paracrine negative regulator of parathyroid cell proliferation and PTH secretion and that loss of TGF-beta signaling due to menin inactivation contributes to parathyroid tumorigenesis.

Authors+Show Affiliations

Division of Endocrinology/Metabolism, Neurology and Hematology/Oncology, Department of Clinical Molecular Medicine, Kobe University Graduate School of Medicine, 7-5-2 Kusunoki-Cho, Chuo-ku, Kobe 650-0017, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15026366

Citation

Sowa, Hideaki, et al. "Menin Inactivation Leads to Loss of Transforming Growth Factor Beta Inhibition of Parathyroid Cell Proliferation and Parathyroid Hormone Secretion." Cancer Research, vol. 64, no. 6, 2004, pp. 2222-8.
Sowa H, Kaji H, Kitazawa R, et al. Menin inactivation leads to loss of transforming growth factor beta inhibition of parathyroid cell proliferation and parathyroid hormone secretion. Cancer Res. 2004;64(6):2222-8.
Sowa, H., Kaji, H., Kitazawa, R., Kitazawa, S., Tsukamoto, T., Yano, S., Tsukada, T., Canaff, L., Hendy, G. N., Sugimoto, T., & Chihara, K. (2004). Menin inactivation leads to loss of transforming growth factor beta inhibition of parathyroid cell proliferation and parathyroid hormone secretion. Cancer Research, 64(6), 2222-8.
Sowa H, et al. Menin Inactivation Leads to Loss of Transforming Growth Factor Beta Inhibition of Parathyroid Cell Proliferation and Parathyroid Hormone Secretion. Cancer Res. 2004 Mar 15;64(6):2222-8. PubMed PMID: 15026366.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Menin inactivation leads to loss of transforming growth factor beta inhibition of parathyroid cell proliferation and parathyroid hormone secretion. AU - Sowa,Hideaki, AU - Kaji,Hiroshi, AU - Kitazawa,Riko, AU - Kitazawa,Sohei, AU - Tsukamoto,Tatsuo, AU - Yano,Shozo, AU - Tsukada,Toshihiko, AU - Canaff,Lucie, AU - Hendy,Geoffrey N, AU - Sugimoto,Toshitsugu, AU - Chihara,Kazuo, PY - 2004/3/18/pubmed PY - 2004/4/9/medline PY - 2004/3/18/entrez SP - 2222 EP - 8 JF - Cancer research JO - Cancer Res VL - 64 IS - 6 N2 - Primary hyperparathyroidism is a common endocrine disorder caused by parathyroid gland enlargement and excessive parathyroid hormone (PTH) secretion. However, the precise mechanisms of tumorigenesis of the parathyroids are unknown. Here we have investigated the roles of transforming growth factor (TGF)-beta and menin, the product of the multiple endocrine neoplasia type 1 (Men1) gene, in the proliferation and PTH production of parathyroid cells from either patients with secondary hyperparathyroidism or Men1. TGF-beta was expressed in the parathyroid endocrine cells. Addition of TGF-beta to parathyroid cells from patients with secondary hyperparathyroidism inhibited their proliferation and PTH secretion. These responses to TGF-beta were lost when menin was specifically inactivated by antisense oligonucleotides. Moreover, TGF-beta did not affect the proliferation and PTH production of parathyroid cells from a Men1 patient. These results indicate that menin is required for TGF-beta action in the parathyroid. We conclude that TGF-beta is an important autocrine/paracrine negative regulator of parathyroid cell proliferation and PTH secretion and that loss of TGF-beta signaling due to menin inactivation contributes to parathyroid tumorigenesis. SN - 0008-5472 UR - https://www.unboundmedicine.com/medline/citation/15026366/Menin_inactivation_leads_to_loss_of_transforming_growth_factor_beta_inhibition_of_parathyroid_cell_proliferation_and_parathyroid_hormone_secretion_ L2 - http://cancerres.aacrjournals.org/cgi/pmidlookup?view=long&pmid=15026366 DB - PRIME DP - Unbound Medicine ER -