• The Journal of Pediatrics of Korean Medicine
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• v.18 no.1
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• pp.11-25
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• 2004

Objectives: These experimental studies were designed to investigate the effects of antler's extracts on the expression of leptin, IGF-l and IGF-1 receptor on cultured 3T3-L1 cells. Methods: A mouse adipoblast cell line, 3T3-L1, was cultured with or without a differentiation medium containing Isobutylmethylxanthin, Dexametasone and Insulin before adding extracts of antler of various concentratio(10, 50, ]00, 200${\mu}g/ml$). The expression of leptin and IGF-1 receptor was measured by western blot assay, and expression of IGF-1 was determined by F ACS analysis. Results and Conclusion: The 3T3-L1 cells' differentiation did not show a significant induction by extracts of antler. The expression of leptin was significantly decreased depend on antler's concentration. The expression of IGF-1 showed a slightly increase by extracts of antler, whereas that of IGF-receptor showed a tendency to increase. The total amount of intracellular triglyceride showed a tendency to diminish as the concentration of antler's extract increase.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.14
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• pp.5753-5757
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• 2014

Background: The purpose of this study is to determine whether the IGF1R expression has a prognostic role in non-small cell lung cancer. Materials and Methods: Forty-seven patients histopathologically diagnosed with small cell lung cancer upon bronchoscopic biopsy or resection materials were included in the study. IGF1R expression was examined via immunohistochemical methods. In samples, >10% staining were assessed as positive and ${\leq}10%$ as negative. Information about demographic datas and treatments was obtained by retrospective searches of patient files. Results: IGF1R expression was determined as positive in 38 (80.9%) and as negative in 9 (19.1%) patients. There was no significant relation between IGF1R expression and histological sub-type, local invasion, lymph node and metastasis status (p=0.842, p=0.437, 0.064, 0.447, respectively). There was also no correlation with IGF1R expression and survival (p=0.141). Conclusions: There are conflicting results between IGF1R and its prognostic effects in the various studies. It has been claimed in some studies it is not related to prognosis as in our study, and in some studies it has been claimed that it is a good prognostic factor whereas in some studies it has been claimed as being a factor for worse prognosis. We think that IGF1R expression in non-small cell lung carcinoma patients deserves further analysis, because of its potential prognostic and predictive roles.

• Development and Reproduction
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• v.2 no.2
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• pp.205-212
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• 1998

A sodium-independent facilitative glucose transporter 1 (Glut1) is a major route by which glucose can be transported across the plasma membrane of mouse embryo. Although it has been known that insulin-like growth factor-I (IGF-I) promotes glucose transport into the mouse embryo, whether IGF-I directly regulates transcription of Glut1 has been uncovered in mouse preimplantation embryo. This study was aimed to elucidate the role of glucose and IGF-I in development and Glut1 expression in preimplantation mouse embryo. Two-cell embryos developed in blastocyst regardless of the glucose in the presence of pyruvate. IGF-I significantly increased the number of blastomeres in the mid-blastula. Deprivation of glucose did not affect the amount of Glut1 transcripts in morula cultured from 2-cell embryo. IGF-I potentiated Glut1 expression in morula cultured from 2-cell embryo even in the absence of glucose. Taken together, it is concluded that depletion of glucose does not promote Glut1 expression the in morula cultured form 2-cell embryo, and that increment of Glut1 expression possibly mediates embryotropic effect of IGF-I on preimplantation mouse embryo.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.10
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• pp.5675-5680
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• 2013

Background: Preexisting type 2 diabetes mellitus (T2DM) affects the prognosis and mortality of patients with some cancers. Insulin like growth factor (IGF) and insulin receptor (IR) signaling axes play important roles in both cancer and diabetes development. We aimed to explore the expression characteristics of proteins in IGF/IR axis in non-small cell lung cancer (NSCLC) cases with preexisting T2DM. Methods: Fifty-five NSCLC patients with preexisting T2DM were retrospectively included and matched by 55 NSCLC without diabetes at a 1:1 ratio. The expression of proteins in IGF/IR axis was detected by immunohistochemical staining. Clinicopathological data were collected to analyze their relationship with the protein expression. Results: Both IGF 1 receptor (IGF-1R) and insulin receptor substrate 2 (IRS-2) showed higher expression in the NSCLC with T2DM group, compared with those without T2DM. The high expression of IGF-1R and IRS-2 were found to be negatively associated with lymph node metastases and T staging in the T2DM group, respectively, and IRS-2 expression was also found more in the subgroup whose T2DM duration was more than 4 years. No difference was detected in the expression of IRS-1, IGF-1, IGF-2, IGFBP3, IR and mTOR between groups with or without T2DM. Conclusion: Our study found higher expression of IGF-1R and IRS-2 proteins in NSCLC patients with preexisting T2DM, and that there was an association with early stage NSCLC, which suggested that IGF signaling may play an important early event in development of NSCLC associated with diabetes.

• Journal of mucopolysaccharidosis and rare diseases
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• v.1 no.2
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• pp.54-59
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• 2015

Purpose: Growth hormone (GH) therapy substantially improves several cognitive functions in PWS. However, the molecular mechanisms underlying the beneficial effects of GH on cognition remain unclear in PWS. In this study, we investigated the effects of recombinant human GH on the gene expression of GABAB receptor subunits and GH/insulin-like growth factor (IGF) axis genes in the brain regions of PWS-mimicking mice (Snord116del). Methods: Snord116del mice were injected subcutaneously with 1.0 mg/kg GH or saline, once daily for 7 days. The collected brain tissues were analyzed for mRNA content using quantitative PCR (qPCR) in the cerebellum, hippocampus, and cerebral cortex. Results: GH increased the mRNA expression level of the $GABA_{B1}$ receptor subunit ($GABA_{BR1}$) and IGF-1R in the cerebellum. Furthermore, a significant positive correlation was found between the level of $GABA_{BR1}$ mRNA and the expression of the IGF-1R transcript. GH also induced an increase in the mRNA expression of IGF-2 and IGF-2R in the cerebellum. Conclusion: These data indicate that GH may provide beneficial effects on cognitive function through its influences on the expression of $GABA_{BR1}$ and GH/IGF-1 axis genes in PWS patients.

• Journal of Life Science
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• v.24 no.12
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• pp.1284-1290
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• 2014

Fatty acid transporter protein 1 (FATP1) is highly expressed in skeletal muscle and modulates fatty acid uptake and metabolism. However, the influence of insulin-like growth factor-I (IGF-I), a master regulator of skeletal muscle cells, on FATP1 in skeletal muscle cells has not been demonstrated. To investigate the effect of IGF-I on FATP1 and the expression of the IGFBP5 protein, differentiated C2C12 murine skeletal muscle cells were treated with 20 ng/ml of IGF-I at different time points. The results showed that IGF-I increased FATP1 and IGFBP5 protein expression in a time-dependent manner. To determine whether this induction of FATP1 by the IGF-I treatment was regulated pretranslationally, the mRNA level of FATP1 was measured by real-time quantitative PCR. The IGF-I treatment resulted in very rapid induction of the FATP1 mRNA transcript in C2C12 myotubes. FATP1 mRNA increased 169% and 132% after 24 and 48 h of the IGF-I treatment, respectively, and it returned to control levels after 72 h of the treatment, suggesting that the FATP1 gene is regulated pretranslationally by IGF-I in skeletal muscle cells. This is the first evidence that IGF-I can regulate the expression of FATP1. In conclusion, IGF-I induced rapid transcriptional modification of the FATP1 gene in C2C12 skeletal muscle cells and had modulating effects on fatty acid uptake proteins and oxidative proteins.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.4
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• pp.1183-1186
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• 2012

Objective: To observe the effect of insulin-like growth factor-1 (IGF-1) on bone morphogenetic protein (BMP)-2 expression in hepatocellular carcinoma SMMC7721 cells. Methods: Cells were divided into blank control, IGF-1, IGF-1 + SB203580, and SB203580 groups. SB203580 was used to block the p38 MAPK signaling pathway. Changes in the expression of BMP-2, p38 MAPK, and phosphorylated p38, MERK, ERK and JNK were determined using reverse transcription polymerase chain reactions (RT-PCR) and Western blot analysis. Results: Protein expression of phosphorylated BMP-2, MERK, ERK, and JNK was significantly up-regulated by IGF-1 compared with the control group ($1.138{\pm}0.065$ vs. $0.606{\pm}0.013$, $0.292{\pm}0.005$ vs. $0.150{\pm}0.081$, $0.378{\pm}0.006$ vs. $0.606{\pm}0.013$, and $0.299{\pm}0.015$ vs. $0.196{\pm}0.017$, respectively; P<0.05). Levels of BMP-2 and phosphorylated MERK and JNK were significantly reduced after blocking of the p38MAPK signaling pathway ($0.494{\pm}0.052$ vs. $0.165{\pm}0.017$, $0.073{\pm}0.07$ vs. $0.150{\pm}0.081$, and $0.018{\pm}0.008$ vs. $0.196{\pm}0.017$, respectively; P<0.05), but such a significant difference was not observed for phosphorylated ERK protein expression ($0.173{\pm}0.07$ vs. $0.150{\pm}0.081$, P>0.05). Conclusion: IGF-1 can up-regulate BMP-2 expression, and p38 MAPK signaling pathway blockage can noticeably reduce the up-regulated expression. We can conclude that the up-regulatory effect of IGF-1 on BMP-2 expression is realized through the p38 MAPK signaling pathway.

• Biomedical Science Letters
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• v.23 no.1
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• pp.39-43
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• 2017

In this study, we evaluated the effects of various hypothermic conditions ($32^{\circ}C$), including lithium chloride treatment, on insulin-like growth factor 1 (IGF-1) gene expression in PC12 cells. The results show that short-term hypothermic treatment (<1 day) resulted in relatively higher IGF-1 gene expression than did longer-term treatment (>1 day). Repeated switching between normal temperature and hypothermia every 2 h increased IGF-1 gene expression approximately 3-4-fold. These findings indicate that hypothermia dynamically regulates IGF-1 gene expression. This study could be helpful for the development of treatment and diagnostic strategies for ischemia.

• BMB Reports
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• v.33 no.6
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• pp.454-462
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• 2000

Interleukin-4(IL-4) is known to be a major cytokine regulating immunoglobulin E(IgE) response by the induction of IgE production and type II IgE receptor(IgER II: CD23) expression. Recently, however, the role of neuroendocrine factors has been implicated in modulating the IgE response. Among various neuroendocrine growth factors, we investigated the effects of the insulin-like growth factor-1(IGF-1) since IL-4 and IGF-1 share common intracellular signaling molecules, such as the insulin receptor substrate-1/2(IRS-1/2) to induce a specific cellular response. In the human peripheral blood mononuclear cell (PBMC) cultures, IGF-1 was capable of inducing a substantial level of IgE production in a dose-dependent manner. It also noticeably upregulated the IL-4-induced or IL-4 plus anti-CD40-induced IgE production. Similarly, the IGF-1-induced IgE production was enhanced by IL-4 or anti-CD40 in an additive manner, which became saturated at high concentrations of IGF-1. Although IGF-1 alone did not induce IgER II (CD23) expression, it augmented the IL-4-induced surface CD23 expression in a manner similar to the action of anti-CD40. These results imply that IGF-1 is likely to utilize common signaling pathways with IL-4 and anti-CD40 to induce IgE and IgER II expression. In support of this notion, we observed that IGF-1 enhanced the IL-4-induced signal transducers and activators of transcription 6(STAT6) activation and independently induced $NF-{\kappa}B$ activation. Both of these bind to the IgE(C) or IgER II (CD23) promoters. Together, our data suggest that IL-4 and IGF-1 work cooperatively to activate STAT6 and $NF-{\kappa}B$. This leads to the subsequent binding of these transcription factors to the $C{\varepsilon}$ and CD23 promoters to enhance the expression of IgE and IgER II. The observed differential ability of IGF-1 on the induction of IgE vs. IgER II is discussed based on the different structure of the two promoters.

• The korean journal of orthodontics
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• v.35 no.5 s.112
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• pp.351-360
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• 2005

This study aimed to investigate the effects of indomethacin on distribution and expression of COX-2 and IGF-1 in the mandibular condyle ofi growing dogs and to examine the number of chondroclasts around the mineralization zone indomethacin inhibits prostatlandin $E_2$ production in the tissue by inhibiting synthesis of cyclooxygenase 2. Prostaglandin $E_2$ stimulates insulin-like growth factor synthesis. Insulin-like growth factor stimulates growth of mandibular condylar cartilage. Eight mongrel dogs. aged 13-14 weeks, were divided into 4 groups. Group 1 and group 2 were administered indomethacin 2 mg/Kg/day orally two times a day for 7 days and 14 days respectively. Group 3 were administered indomethacin 8mg/Kg/day orally 2 times a day for 14 days, and 4he control group were administered a placebo. The mandibular condyle heads were sectioned in $5{\mu}m$ thickness The specimens were stained with H-E staining. COX-2 immunohistochemical staining and IGF-1 immunohistochemical staining and examined under microscope. After TRAP staining, the number of chondroclasts were calculated The observed results were as follows: Indomethacin inhibited expression and distribution of COX-2 and IGF-1 on the proliferative zone of condylar cartillage. Indomethacin decreased the number of chondroclastes on the mineralization zone by a time-dependent manner (P<0.05). Indomethacin inhibited expression and distribution of IGF-I by a dose and time-dependent manner. These results show that indomethacin inhibited expression and distribution of COX-2 and IGF-1 on the proliferative zone of condylar cartilage and decreased the number of chondroclasts and suggests that when indomethacin is administered for a long time, condyle growth could be delayed.