Epidermal growth factor stimulates cell proliferation and inhibits iodide uptake of FRTL-5 cells in vitro

Asmis, Lars M.; Gerber, H.; Kaempf, Jacqueline; Studer, H

doi:10.1677/joe.0.1450513

Cited by 22 publications

(19 citation statements)

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“…Despite the fact that FRTL-5 cells have been extensively used for many years, the mechanism regulating their (23). It should be pointed out that an EGF effect has been described mainly in aged cells; this could indeed be the case in the current investigation, as commented upon below.…”

Section: Discussionmentioning

confidence: 65%

Insulin and TSH promote growth in size of PC Cl3 rat thyroid cells, possibly via a pathway different from DNA synthesis: comparison with FRTL-5 cells

Kimura¹,

Dumont²,

Fusco

et al. 1999

European Journal of Endocrinology

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In the rat thyroid cell lines PC Cl3, FRTL-5 and WRT, proliferation is mainly regulated by insulin or IGF, and TSH. However, the mechanism regulating cell mass doubling prior to division is still unknown. Our laboratory has shown that in dog thyroid cells insulin promotes growth in size while TSH in the presence of insulin triggers DNA replication. In the absence of insulin, TSH has no effect on cell growth. In this report we investigated insulin action on both cell mass and DNA synthesis and its modulation by TSH and insulin in PC Cl3 and FRTL-5 cells. In PC Cl3 cells, insulin activated not only DNA synthesis but also protein synthesis and accumulation. Although TSH potentiated the stimulation of DNA synthesis induced by insulin, enhancement of protein synthesis by both agents was additive. All TSH effects were reproduced by forskolin. Similar effects were also obtained in FRTL-5 cells. This suggests that insulin and TSH, via cAMP, modulate both growth in size and DNA replication in these cell lines.Lovastatin, which blocks 3-hydroxy-3-methylglutaryl coenzyme A reductase, decreased the induction of DNA synthesis, but not of protein synthesis induced by insulin or TSH in PC Cl3 cells. In FRTL-5 cells, lovastatin reduced protein and DNA synthesis stimulated by insulin but not TSH-induced protein synthesis. Taking these data together, we propose that insulin and/or TSH both modulate cell mass doubling and DNA synthesis in these cell lines, presumably via different pathways, and that there are at least two pathways which regulate growth in size in FRTL-5 thyroid cells: one triggered by insulin, which is lovastatin sensitive, and the other activated by TSH, which is not sensitive to lovastatin.

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Section: Discussionmentioning

confidence: 65%

Insulin and TSH promote growth in size of PC Cl3 rat thyroid cells, possibly via a pathway different from DNA synthesis: comparison with FRTL-5 cells

Kimura¹,

Dumont²,

Fusco

et al. 1999

European Journal of Endocrinology

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“…The differential expression of these critical genes and their downstream effectors enables cells to override growth controls and eventually undergo carcinogenesis. Mutations of p53 [3], RAS [4], and B-RAF [5], rearrangement of PPARG [6] and RET/PTC [7], and amplification and overexpression of FGFR and EGFR [8] have been observed in thyroid cancer. However, the precise mechanisms of thyroid cancer at the molecular level are still poorly understood.…”

Section: Introductionmentioning

confidence: 99%

CTGF is overexpressed in papillary thyroid carcinoma and promotes the growth of papillary thyroid cancer cells

et al. 2011

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Connective tissue growth factor (CTGF or CCN2), which belongs to the CCN family, is a secreted protein. It has been implicated in various biological processes, such as cell proliferation, migration, angiogenesis, and tumorigenesis. In this study, we found that CTGF expression level was elevated in primary papillary thyroid carcinoma (PTC) samples and correlated with clinical features, such as metastasis, tumor size, and clinical stage. Overexpression of CTGF in PTC cells accelerated their growth in liquid culture and soft agar as well as protecting PTC cells from apoptosis induced by IFN-gamma treatment. Downregulation of CTGF in PTC cells inhibits cell growth in liquid culture and soft agar and induces the activation of caspase pathway and sensitized PTC cells to apoptosis. Our data suggest that CTGF plays an important role in PTC progression by supporting tumor cell survival and drug resistance, and CTGF may be used as a potential tumor marker for PTC diagnosis.

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“…many studies have reported on the regulation of thyroid cell proliferation by TSh [9], insulin/insulinlike growth factor i (iGF-i) [10,11], and other growth factors, including fibroblast growth factor-2 (FGF-2) [12] and epidermal growth factor [13]. These studies were conducted by using various cell culture systems, such as primary cultures of rat, dog, sheep and human thyroid cells as well as using rat thyroid cell lines, such as FRTL-5, WRT, and Pc cl3.…”

Section: Preparation and Primary Culture Of Porcine Thyroid Epitheliamentioning

confidence: 99%

Proliferative Effects of Bovine and Porcine Thyroglobulins on Thyroid Epithelial Cells

et al. 2009

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Epidermal growth factor stimulates cell proliferation and inhibits iodide uptake of FRTL-5 cells in vitro

Cited by 22 publications

References 0 publications

Insulin and TSH promote growth in size of PC Cl3 rat thyroid cells, possibly via a pathway different from DNA synthesis: comparison with FRTL-5 cells

Insulin and TSH promote growth in size of PC Cl3 rat thyroid cells, possibly via a pathway different from DNA synthesis: comparison with FRTL-5 cells

CTGF is overexpressed in papillary thyroid carcinoma and promotes the growth of papillary thyroid cancer cells

Proliferative Effects of Bovine and Porcine Thyroglobulins on Thyroid Epithelial Cells

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