Thyrotropin induces G1 cyclin expression and accelerates G1 phase after insulin-like growth factor I stimulation in FRTL-5 cells

Yamamoto, Kaori

doi:10.1210/en.137.5.2036

Cited by 21 publications

(32 citation statements)

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“…Furthermore, inhibition of cyclin D3 function induced by neutralizing antibodies suppressed TSH-dependent proliferation of dog thyrocytes Wollman et al, 1978). Conversely, in another rat cell line (the FRTL-5 cells), TSH-dependent proliferation occurs both through upregulation of D-type cyclins and downregulation of the cyclin-dependent kinase inhibitor p27 kip1 (Yamamoto et al, 1996;Carneiro et al, 1998;Medina et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Critical role of cyclin D3 in TSH-dependent growth of thyrocytes and in hyperproliferative diseases of the thyroid gland

Motti

Boccia

Belletti³

et al. 2003

Oncogene

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We report that cyclin D3 is rate limiting for G1 progression in thyroid follicular cells and that its constitutive upregulation by chronic stimulation of the TSH/cAMP pathway plays a role in human and experimental hyperproliferative diseases of the thyroid gland. These conclusions are supported by in vitro and in vivo studies. In rat thyrocytes (PC Cl 3 cells), cyclin D3 expression is enhanced in response to activation of the TSH/cAMP pathway. Interference with the expression of G1 cyclins (in particular cyclin D3) by the antisense methodology strongly reduced TSH-dependent proliferation of PC Cl 3 cells, indicating that proper progression through G1 requires cyclin D3. Accordingly, PC Cl 3 cells engineered to overexpress cyclin D3 (PC-D3 cells) show enhanced growth rate and elude hormone-dependence and contact inhibition. Using an animal experimental model of thyroid stimulation, we demonstrate that cyclin D3 is a key mediator of TSH-dependent proliferation of thyroid follicular cells also in vivo. Cyclin D3 protein levels were higher in the thyrocytes from glands of propylthiouraciltreated rats compared with control animals. The increase in cyclin D3 expression occurred after the propylthiouracil-induced increase in TSH levels and preceded the burst of cell proliferation. Finally, we found that cyclin D3 protein is expressed in a fraction of human goiters but it is strongly overexpressed in most follicular adenomas.

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Section: Introductionmentioning

confidence: 99%

Critical role of cyclin D3 in TSH-dependent growth of thyrocytes and in hyperproliferative diseases of the thyroid gland

Motti

Boccia

Belletti³

et al. 2003

Oncogene

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“…However, cyclic AMP induces cyclin D1 in other cells (Yamamoto et al, 1996). These opposite regulations might involve the CRE in the promoter of the cyclin D1 gene.…”

Section: Effects Of Cyclic Amp On Cyclins and Cdks In Astrocytesmentioning

confidence: 98%

“…Cyclic AMP activates PKA, which phosphorylates various substrates, including CRE binding proteins, that take part in the regulation of the expression of various genes. As the promoters of cyclins D1 and A contain a CRE (Desdouets et al, 1995;Yamamoto et al, 1996), cyclic AMP can block the expression of these cyclins via phosphorylation of CRE binding proteins by PKA. To our knowledge, CREs have not been found in the promoters of cdk1 and cdk2.…”

Section: Figmentioning

confidence: 99%

“…Cyclin E is induced by cyclic AMP in several systems (Yamamoto et al, 1996), but it is repressed in others, such as oligodendrocytes (Friessen et al, 1997) and C.LT.T.1.1 cells .…”

Section: Effects Of Cyclic Amp On Cyclins and Cdks In Astrocytesmentioning

confidence: 99%

“…Cyclic AMP increases the accumulation of a cki, p27 KIP1 , in murine macrophages (Kato et al, 1994) and in oligodendrocytes (Friessen et al, 1997), and it stimulates the expression of cyclin A mRNA in human fibroblasts by acting on a cyclic AMPresponsive element (CRE) in the gene promoter (Desdouets et al, 1995). It induces cyclins D1 and E in FRTL5 cells (Yamamoto et al, 1996), but it reduces cyclin D1 in other cellular models (Cocks et al, 1992;Sewing et al, 1993;Herber et al, 1994). Little information is available on the cell cycle apparatus and its control in astrocytes.…”

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Effects of Cyclic AMP on Components of the Cell Cycle Machinery Regulating DNA Synthesis in Cultured Astrocytes

Gagelin

Toru-Delbauffe²,

Gavaret³

et al. 1999

Journal of Neurochemistry

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Cyclic AMP is a second messenger for various hormones that inhibits cell multiplication and DNA synthesis in cultured astrocytes. We examined the effects of increasing intracellular cyclic AMP on the catalytic (cdks) and regulatory (cyclins and ckis) components of cyclindependent protein kinases, which regulate progression of the cell cycle before completion of DNA synthesis, in primary cultured astrocytes and in an astrocytic cell line C.LT.T.1.1. The amount of cdk4 changed little during the cell cycle and was not affected by cyclic AMP. There was little cdk1 and cdk2 in quiescent cells, and their expression increased during the G 1 -S phases. Cyclic AMP strongly inhibited cdk1 and cdk2 expression. Transforming growth factor ␤ also inhibited cdk1 expression in primary astrocytes. Cyclic AMP did not affect the two ckis p27 KIP1 and p21 CIP1 . There was little cyclin D1 in quiescent cells, but it increased during the G 1 phase and was reduced by cyclic AMP. Cyclin E increased during the G 1 -S phases and was not affected by cyclic AMP in primary astrocytes. The amount of cyclin A was low in quiescent cells and increased during the G 1 -S phases. Expression of its mRNA and protein was inhibited by cyclic AMP. The protein kinase activities associated with complexes of cyclins and cdks were increased by growth factors and prevented by cyclic AMP. We conclude that cyclic AMP inhibits progression of the cell cycle in astrocytes at least by preventing the expression of the regulatory subunits, cyclins D1 and A, and catalytic subunits, cdk1 and cdk2, of cyclin-regulated protein kinases.

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Role of p27Kip1 and Cyclin-Dependent Kinase 2 in the Proliferation of Non-Small Cell Lung Cancer

Kawana

Tamaru

Tanaka

et al. 1998

The American Journal of Pathology

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The cell cycle is governed by a family of cyclin-dependent kinases (Cdks). Cdk2 forms a functional complex with cyclin E and plays a pivotal role in the regulation of G1/S transition. Cdk2 activity is negatively regulated by interactions with inhibitors. p27 Kip1 , one of the most potent inhibitors of Cdk2, was recently identified as a powerful negative prognostic marker in non-small cell lung cancer as well as in colorectal and breast cancer. In the present study, the expression of p27 and Ki-67 antigen in nonneoplastic and cancerous lung tissues was determined by immunohistochemistry. After establishing that the antibody-measured p27 labeling index was a good reflection of the level of p27 expression measured by Western blotting , we show that p27 labeling index is decreased in cancerous lung tissues , compared with nonneoplastic lung tissues , and exhibits a significant inverse relation to the proliferation marker Ki-67 antigen , detected with monoclonal antibody MIB-1. Consistent with these data , all cancerous lung tissues showed enhanced degradation activity of p27 compared with nonneoplastic lung tissues and , in addition , increased levels of the phosphorylated form of Cdk2 , as determined with Western blot analysis. The H1 histone kinase activity associated with Cdk2 was also increased in non-small cell lung cancers. Statistical analysis showed that proliferative activity as measured by MIB-1 labeling index was highly correlated with Cdk2 activity (r ‫؍‬ 0.767 , P < 0.0015). These results suggest that p27 and Cdk2 may play an important role in the proliferation of non-small cell cancer. (Am J Pathol 1998, 153:505-513)

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Thyrotropin induces G1 cyclin expression and accelerates G1 phase after insulin-like growth factor I stimulation in FRTL-5 cells

Cited by 21 publications

References 0 publications

Critical role of cyclin D3 in TSH-dependent growth of thyrocytes and in hyperproliferative diseases of the thyroid gland

Critical role of cyclin D3 in TSH-dependent growth of thyrocytes and in hyperproliferative diseases of the thyroid gland

Effects of Cyclic AMP on Components of the Cell Cycle Machinery Regulating DNA Synthesis in Cultured Astrocytes

Role of p27Kip1 and Cyclin-Dependent Kinase 2 in the Proliferation of Non-Small Cell Lung Cancer

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