Thyrotropin (TSH) stimulates cell growth and DNA synthesis in monolayer cultures of human thyrocytes independent of the adenylate-cyclase system

1987 ◽  
Vol 116 (1_Suppl) ◽  
pp. S273-S280 ◽  
Author(s):  
Peter E. Goretzki ◽  
Rainer Koob ◽  
Christine Koller ◽  
Hans-Dietrich Röher
Keyword(s):  
Thyroid Cancer ◽  
Cell Growth ◽  
Adenylate Cyclase ◽  
Dna Synthesis ◽  
Thymidine Incorporation ◽  
Human Thyroid ◽  
Adenylate Cyclase System ◽  
Monolayer Cultures ◽  
Cancer Metastases ◽  
Thyroid Adenomas

Abstract. Monolayer cultures of human thyrocytes from normal thyroids (n = 13), thyroid adenomas (n = 8), differentiated (n = 7), poorly and undifferentiated (n = 5) thyroid cancers as well as thyroid cancer metastases (n = 2) were established to assess the significance of TSH and cAMP on cell growth and DNA synthesis. Cell growth was stimulated by 0.1 IU bTSH/ml and inhibited by 1.0 IU bTSH/ml (P < 0.01), while dibutyryl-cAMP (dbcAMP) failed to show any effect on cell growth at the concentrations (10–5; 10–3 mol/l), tested. Neither did the adenylate-cyclase inhibitor dideoxy-adenosine (ddA) (2 × 10–5 mol/l) stimulate thyrocyte growth. DNA synthesis, however, measured indirectly by [3H]thymidine incorporation, was stimulated not only by TSH 2–12-fold, but also by ddA 1.3–7-fold (P <0.01), and was not affected by dbcAMP. TSH had no effect on [3H]thymidine incorporation in fibroblasts and c-cells from c-cell carcinomas. The stimulatory effect of TSH on thyrocyte growth and DNA synthesis was unpredictable in thyrocytes from cancerous tissues (n = 14) with no obvious correlation to tumour differentiation or stage. Thus, we showed that TSH is a promotor for cell growth and DNA synthesis in monolayer cultures of human thyrocytes from normal and adenomatous human thyroid tissues with no obvious correlation to the AC system. This TSH effect is unpredictable, however, in thyrocytes from human thyroid cancer.

Effects Of Aspirin And Sulfinpyrazone On Platelets, Vascular Cells And Their Interactions

1981 ◽  
Author(s):  
M R Buchanan ◽  
M J Vazquez ◽  
M A Gimbrone
Keyword(s):  
Growth Rate ◽  
Cell Growth ◽  
Dna Synthesis ◽  
Vessel Wall ◽  
Culture Medium ◽  
Platelet Adhesion ◽  
Thymidine Incorporation ◽  
Inhibitory Effect ◽  
Human Platelets ◽  
Final Density

Sulfinpyrazone (SUL) and aspirin (ASA) are potentially useful antithrombotic drugs. Both drugs are thought to exert this effect by inhibiting the platelet enzyme, cyclooxygenase (C-0), thus preventing thromboxane A2 synthesis. Recent data, however, suggest that these drugs also may affect vessel wall cells. To study this further, we examined the effects of SUL and ASA on i) the adhesion of 3H-adenine-labelled washed human platelets to cultured bovine endothelial (EC) and smooth muscle cells (SMC), ii) EC and SMC DNA synthesis (3H-thymidine incorporation) and iii) cell growth. Pretreatment of platelets with 100μM ASA or 250μM SUL (concentrations sufficient to inhibit C-0), did not affect platelet adhesion to untreated EC or SMC. However, adhesion of untreated, ASA- and SUL-platelets was increased 25,28 and 44% resp. when EC were pretreated with 650μM SUL for 24 hr. In contrast, adhesion of ASA-platelets to EC pretreated with lOOμM ASA (sufficient to inhibit prostacyclin), was unaffected. Platelet adhesion to SMC pretreated with 650μM SUL for 24 hr was decreased when platelets also were pretreated with ASA (20%, p<0.05) or SUL (27%, pc 0.02). Pretreatment of SMC with SUL for only 2 hr had no effect. DNA synthesis in EC and SMC treated with 62.5 and 250μM SUL for 24 hr, was inhibited >35% and >95% resp. Preliminary data suggest that this inhibitory effect may last longer in SMC. To study the effect of SUL on cell growth, EC and SMC were plated at 2 × 104 cells/ cm2 and fed with culture medium containing 0, 62.5 or 625uM SUL on day 0, 1, 3 and 4.5. EC growth rate and final density were unaffected over 7 days. SMC growth rate also was unaffected, but the final density of SMC treated with 650μM SUL was 31 μ 2% less than untreated SMC at 7 days (p<0.01). These data indicate that SUL has direct effects on EC and SMC that may influence i) platelet-vessel wall interactions and ii) vascular cell proliferation.

scholarly journals miR-429 suppresses cell growth and induces apoptosis of human thyroid cancer cell by targeting ZEB1

2019 ◽  
Vol 47 (1) ◽  
pp. 548-554 ◽  
Author(s):  
Guochang Wu ◽  
Haitao Zheng ◽  
Jie Xu ◽  
Yawen Guo ◽  
Guibin Zheng ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Human Thyroid ◽  
Thyroid Cancer Cell

Effects of prostaglandin E2 and TSH on adenylate cyclase system of intact human thyroid cells

1978 ◽  
Vol 16 (5) ◽  
pp. 749-757 ◽  
Author(s):  
Annalisa Tanini ◽  
Stefano Aterini ◽  
Patrizia Fani ◽  
Carlo M. Rotella ◽  
Roberto Toccafondi
Keyword(s):  
Adenylate Cyclase ◽  
Prostaglandin E2 ◽  
Human Thyroid ◽  
Adenylate Cyclase System ◽  
Thyroid Cells

scholarly journals Effect of 22-Oxa-1,25-Dihydroxyvitamin D3 on Human Thyroid Cancer Cell Growth.

1999 ◽  
Vol 46 (2) ◽  
pp. 243-252 ◽  
Author(s):  
KUNIHIKO OKANO ◽  
TOSHIRO USA ◽  
AURA OHTSURU ◽  
TOMOO TSUKAZAKI ◽  
YOUICHI MIYAZAKI ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Human Thyroid ◽  
Thyroid Cancer Cell ◽  
Cancer Cell Growth ◽  
Dihydroxyvitamin D3 ◽  
1,25 Dihydroxyvitamin D3

Prostacyclin stimulates the adenylate cyclase system of human thyroid tissue

1981 ◽  
Vol 22 (1) ◽  
pp. 105-115 ◽  
Author(s):  
C. Patrono ◽  
C.M. Rotella ◽  
R.S. Toccafondi ◽  
S. Aterini ◽  
E. Pinca ◽  
...  
Keyword(s):  
Adenylate Cyclase ◽  
Thyroid Tissue ◽  
Human Thyroid ◽  
Adenylate Cyclase System ◽  
Human Thyroid Tissue

scholarly journals Neuronal inhibition of astroglial cell proliferation is membrane mediated.

1987 ◽  
Vol 104 (5) ◽  
pp. 1353-1360 ◽  
Author(s):  
M E Hatten
Keyword(s):  
Cell Growth ◽  
Dna Synthesis ◽  
Thymidine Incorporation ◽  
Membrane Preparation ◽  
Specific Cell ◽  
Granule Neurons ◽  
Astroglial Cell ◽  
Membrane Interactions ◽  
Astroglial Cells ◽  
Neuronal Inhibition

Previously we have used a microwell tissue culture assay to show that early postnatal mouse cerebellar astroglia have a flattened morphology and proliferate rapidly when they are cultured in the absence of neurons, but develop specific cell-cell contacts and undergo morphological differentiation when they are co-cultured with purified granule neurons (Hatten, M. E., 1985, J. Cell Biol., 100:384-396). In these studies of cell binding between neurons and astroglia, measurement with light and fluorescence microscopy or with [35S]methionine-labeled cells indicated that the kinetics of the binding of the neurons to astroglial cells are rapid, occurring within 10 min of the addition of the neurons to the growing glia. 6 h after neuronal attachment, astroglial DNA synthesis decreases, as shown by a two- to fivefold decrease in [3H]thymidine incorporation, and glial growth ceases. No effects on astroglial cell growth were seen after adding medium conditioned by purified cerebellar neurons cultured in the absence of astroglia, by astroglia cultured in the absence of neurons, or by a mixed population of cerebellar cells. This result was unchanged when any of these media were concentrated up to 50-fold, or when neurons and astroglia were cultured in separate chambers with confluent medium. Two groups of experiments suggest that membrane-membrane interactions between granule neurons and astroglia control astroglial cell growth. First, neurons fixed with dilute amounts of paraformaldehyde (0.5%) bound to the astroglia with the same kinetics as did living cells, inhibited DNA synthesis, and arrested glial growth within hours. Second, a cell membrane preparation of highly purified granule neurons also bound rapidly to the glia, decreased [3H]thymidine incorporation two- to fivefold and inhibited astroglial cell growth. The rate of the decrease in glial growth depended on the concentration of the granule neural membrane preparation added. A similar membrane preparation from purified cerebellar astroglial cells, PC12 cells, 3T3 mouse fibroblasts, or PTK rat epithelial cells did not decrease astroglial cell growth rates. Living neurons were the only preparation that both inhibited glial DNA synthesis and induced the astroglial cells to transform from the flat, epithelial shapes they have when they are cultured without neurons to highly differentiated forms that resemble Bergmann glia or astrocytes seen in vivo. These results suggest that membrane-membrane interactions between neurons and astroglia inhibit astroglial proliferation in vitro, and raise the possibility that membrane elements involved in glial growth regulation include neuron-glial interaction molecules.

Human Thyroid Cancer: Membrane Thyrotropin Binding and Adenylate Cyclase Activity

1980 ◽  
Vol 51 (4) ◽  
pp. 915-920 ◽  
Author(s):  
PIERRE CARAYON ◽  
COLETTE THOMAS-MORVAN ◽  
ELIAS CASTANAS ◽  
MAURICE TUBIANA
Keyword(s):  
Thyroid Cancer ◽  
Adenylate Cyclase ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Human Thyroid

scholarly journals Targeting the TSH receptor in thyroid cancer

2017 ◽  
Vol 24 (6) ◽  
pp. R191-R202 ◽  
Author(s):  
Christopher W Rowe ◽  
Jonathan W Paul ◽  
Craig Gedye ◽  
Jorge M Tolosa ◽  
Cino Bendinelli ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Molecular Basis ◽  
Risk Profile ◽  
Thyroid Stimulating Hormone ◽  
Human Thyroid ◽  
Oncogenic Pathway ◽  
Cancer Metastases ◽  
Thyroid Cancer Metastases ◽  
Metastatic Thyroid Cancer ◽  
Stimulating Hormone

Recent advances in the arena of theranostics have necessitated a re-examining of previously established fields. The existing paradigm of therapeutic thyroid-stimulating hormone receptor (TSHR) targeting in the post-surgical management of differentiated thyroid cancer using levothyroxine and recombinant human thyroid-stimulating hormone (TSH) is well understood. However, in an era of personalized medicine, and with an increasing awareness of the risk profile of longstanding pharmacological hyperthyroidism, it is imperative clinicians understand the molecular basis and magnitude of benefit for individual patients. Furthermore, TSHR has been recently re-conceived as a selective target for residual metastatic thyroid cancer, with pilot data demonstrating effective targeting of nanoparticles to thyroid cancers using this receptor as a target. This review examines the evidence for TSHR signaling as an oncogenic pathway and assesses the evidence for ongoing TSHR expression in thyroid cancer metastases. Priorities for further research are highlighted.

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