Expression of Insulin‐like Growth Factor I (IGF‐I) Gene and of Genes for IGF‐Binding Proteins 1, 2, 3, 4 (IGFBP‐1—IGFBP‐4) in Non‐neoplastic Human Thyroid Cells and in Certain Human Thyroid Cancers. Effect of Exogenous IGF‐I on This Expression

Lewiński, Andrzej; Marcinkowska, Magdalena; Brzeziańska, Ewa; Jeziorowska, Anna; Włoch, Jan; Brzeziński, Jan

doi:10.1081/erc-120028484

Cited by 13 publications

(13 citation statements)

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“…The presence of IGF-I receptors was shown in both normal and neoplastic thyroid tissue in humans, a long time ago. There are numerous scientific evidence that IGF-I reveals an important, TSH–independent effect in growth processes in humans thyroid [ 2 , 3 ]. Moreover, there are a lot of studies describing the increased prevalence of goitre (both diffuse and nodular) in acromegalic patients, and many authors have demonstrated a positive correlation between the thyroid volume and serum IGF-I concentration.…”

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confidence: 99%

Acromegaly and the thyroid gland

Lewiński

Marcinkowska

2015

Thyroid Research

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confidence: 99%

Acromegaly and the thyroid gland

Lewiński

Marcinkowska

2015

Thyroid Research

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“…IGFBP4 is produced mainly in the liver but many other tissues, especially neoplastic tissue, produce it (Korc-Grodzicki et al, 1993;Lewinski et al, 2004).…”

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Expression of a protease-resistant insulin-like growth factor-binding protein-4 inhibits tumour growth in a murine model of breast cancer

et al. 2009

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BACKGROUND: Insulin-like growth factor 1 (IGF1) promotes breast cancer and disease progression. Bioavailability of IGF1 is modulated by IGF-binding proteins (IGFBPs). IGFBP4 inhibits IGF1 activity but cleavage by pregnancy-associated plasma protein-A (PAPP-A) protease releases active IGF1. METHODS: Expression of IGF pathway components and PAPP-A was assessed by western blot or RT -PCR. IGFBP4 (dBP4) resistant to PAPP-A cleavage, but retaining IGF-binding capacity, was used to block IGF activity in vivo. 4T1.2 mouse mammary adenocarcinoma cells transfected with empty vector, vector expressing wild-type IGFBP4 or vector expressing dBP4 were implanted in the mammary fat pad of BALB/c mice and tumour growth was assessed. Tumour angiogenesis and endothelial cell apoptosis were assessed by immunohistochemistry. RESULTS: 4T1.2 cells expressed the IGF1R receptor and IGFBP4. PAPP-A was expressed within mammary tumours but not by 4T1.2 cells. Proliferation and vascular endothelial growth factor (VEGF) production by 4T1.2 cells was increased by IGF1(E3R) (recombinant IGF1 resistant to binding by IGFBPs) but not by wild-type IGF1. IGF1-stimulated microvascular endothelial cell proliferation was blocked by recombinant IGFBP4. 4T1.2 tumours expressing dBP4 grew significantly more slowly than controls or tumours expressing wild-type IGFBP4. Inhibition of tumour growth by dBP4 was accompanied by the increased endothelial cell apoptosis. CONCLUSION: Protease-resistant IGFBP4 blocks IGF activity, tumour growth and angiogenesis .

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“…via enzymes involved in DNA synthesis [40]. Furthermore, IGF-I may contribute to thyroid cancers development [41]. Therefore, the somatotrophic signaling can also be reduced in this endocrine gland in dwarf mice, what may, presumably, lead to the decrease of the examined thyroid morphological parameters.…”

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Decreased thyroid follicle size in dwarf mice may suggest the role of growth hormone signaling in thyroid growth regulation

et al. 2012

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BackgroundAltered somatotrophic signaling is among the most important potential mechanisms of extended longevity. Ames dwarf (df/df) mice are homozygous for mutation at the Prop-1 gene, leading to a lack of growth hormone (GH), prolactin and thyroid stimulating hormone (TSH). Mice homozygous for targeted disruption of the growth hormone receptor/growth hormone binding protein gene are known as GH receptor knockout (GHRKO) mice or “Laron dwarf”. Both, df/df and GHRKO mice, are characterized by reduced body size, low plasma insulin and insulin-like growth factor-I (IGF-I), remarkably extended longevity, and severe (in df/df mice) or mild (in GHRKO mice) thyroid hypofunction. Recently, by crossing df/df and GHRKO mice, double-mutant Ames dwarf/GHRKO (df/KO) mice were created. Interestingly, these mice are smaller than Ames dwarfs or GHRKOs, and also have reduced insulin and IGF-I levels. The aim of the study was to investigate if and to what extent certain thyroid morphological parameters, such as inner follicular surface area, inner follicular perimeter, as well as the follicular epithelium thickness are changed in the examined dwarf mice.MethodsThis quantification was performed in thyroids collected from df/df, GHRKO and df/KO female mice, at approximately 5–6 months of age. We used a computerized plotting programme that combines a live microscopic image of the slide with an operator-generated overlay.ResultsInner follicular surface area and inner follicular perimeter were decreased in all examined kinds of dwarf mice as compared to normal animals. Furthermore, decreases in these two parameters were more pronounced in df/df and df/KO than in GHRKO mice. Concerning the follicular epithelium thickness, only a tendency towards decrease of this parameter was found in all three kinds of dwarf mice.ConclusionsParameters characterizing thyroid follicle size are decreased in all three examined models of dwarf mice, which may explain decreased thyroid hormone levels in both basal mutants (Ames dwarfs and GHRKOs). df/df mutation seems to predominate over GHRKO genetic intervention concerning their effects on thyroid growth. Beside TSH, also GH signaling seems to constitute a crucial element in the regulation of thyroid growth and, possibly, function.

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Expression of Insulin‐like Growth Factor I (IGF‐I) Gene and of Genes for IGF‐Binding Proteins 1, 2, 3, 4 (IGFBP‐1—IGFBP‐4) in Non‐neoplastic Human Thyroid Cells and in Certain Human Thyroid Cancers. Effect of Exogenous IGF‐I on This Expression

Cited by 13 publications

References 20 publications

Acromegaly and the thyroid gland

Acromegaly and the thyroid gland

Expression of a protease-resistant insulin-like growth factor-binding protein-4 inhibits tumour growth in a murine model of breast cancer

Decreased thyroid follicle size in dwarf mice may suggest the role of growth hormone signaling in thyroid growth regulation

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