• Journal of Korean Neurosurgical Society
• /
• v.29 no.6
• /
• pp.731-737
• /
• 2000

Objective : Growth factor receptors on the tumor cells are known to be expressed highly allowing the tumor cells to bind growth factors to stimulate cellular division. Immunotoxin therapy is one of the novel approaches to the primary malignant brain tumor, and expression of cell-surface receptor is essential for the immunotoxin to have specific anti-tumor activity. Despite promising cytotoxic activity of immunotoxin, tumor responses are not curative on clinical trials, and additional studies are needed regarding various factors influencing the efficacy of the immunotoxin. The purpose of this study is to detect the expression of various growth factor receptors on brain tumor cell lines which are going to be used in these studies. Materials and Methods : The authors detected transferrin receptor(TR), insulin-like growth factor-1 receptor(IGF-1R), and interleukin-4 receptor(IL-4R) on medulloblastoma cell line(Daoy) and glioblastoma cell lines(U373 MG and T98 G) by flow cytometric analysis. Results : TR was expressed on Daoy, U373 MG, and T98 G. IGF-1R was expressed on Daoy and U373 MG, but not on T98 G. IL-4R was expressed on all cell lines tested. Conclusion : The transferrin and interleukin-4 receptors might be good targets for immunotoxin therapy. The results should be considered in additional in vitro and in vivo studies regarding immunotoxin and in establishing the proper treatment model of the immunotoxin therapy including selection of the adequate immunotoxin.

• Korean journal of applied entomology
• /
• v.61 no.1
• /
• pp.85-90
• /
• 2022

Insulin and insulin-like growth factor-1 (IGF-1) are hormones that play an important role in the physiological regulation of metabolism, growth, and longevity in vertebrates. Likewise, insulin-like peptides (ILPs), which are structurally similar to insulin and IGF-1, are crucial in insect physiology. In this review, we present an integrated summary of insect ILPs and their receptor signaling, which has been shown to be comparable to insulin and IGF-1 receptor signaling in vertebrates based on genetic studies of Drosophila melanogaster. Additionally, we review the control of ILP synthesis and secretion in the brain in response to nutrition, as well as the ILPs' physiological role in insect metabolism. Moreover, we discuss the contribution of ILPs to growth, development, reproduction, and diapause. Finally, we consider the possibility of targeting ILP receptor signaling in pest management.

• Development and Reproduction
• /
• v.3 no.1
• /
• pp.69-74
• /
• 1999

Insulin-like growth factors (IGF-1 and IGF-2) play an important regulatory role in premplantation embryonic development. To study the role of IGF-1 during premplantation embryonic development in mouse, the presence of mRNA transcripts for IGF-1 and IGF-lR in the oocytes and preimplantation embryos was examined. In this study, the transcripts of IGF-1 was detected in oocytes using primers for IGF-1. The PCR products were identified by Msp I restriction enzyme digest. We revealed that the transcripts of IGF-1 and IGF-1R were presented in the oocytes and preimplantation embryos. The highest mRNA levels in GV stage oocytes were decreased at 4- or 8-cell stage and then reincreased upto blastocyst. The presence of IGF-1 and IGF-lR in GV-oocytes suggests that the transcripts in the early stage embryos were derived from maternal genome. Additionally, the presence of IGF-1 and IGF-lR in the oocytes and preimplantation embryos suggests that IGF-1 plays an autocrine role during preimplantation embryonic development through IGF-lR as a signalling pathway.

• Journal of Life Science
• /
• v.21 no.2
• /
• pp.242-250
• /
• 2011

Although insulin-like growth factor-I (IGF-I) and androgen receptor (AR) coactivators are well known effectors of skeletal muscle, the molecular mechanism by which signaling pathways integrating AR coactivators and IGF-I in skeletal muscle cells has not been previously examined. In this study, the effects of IGF-I treatment on the gene expression of AR coactivators in the absence of AR ligands and the roles of the p38 MAPK and ERK1/2 signaling pathways in IGF-I-induced AR coactivators induction were examined. C2C12 cells were treated with 250 ng/ml of IGF-I in the presence or absence of specific inhibitors p38 MAPK (SB203580) or ERK1/2 (PD98059). Treatment of C2C12 cells with IGF-I resulted in increased in GRIP-1, SRC-1, and ARA70 protein expression. The levels of GRIP-1, SRC-1, and ARA70 mRNA were also significantly increased after 5min of IGF-I treatment. IGF-I-induced AR coactivator proteins were significantly blocked by pharmacological inhibitors of p38 MAPK and ERK1/2 pathways. However, there was no significant effect of those inhibitors on IGF-I-induced mRNA level of AR coactivators, suggesting that AR coactivators are post-transcriptionally regulated by IGF-I. Furthermore, the present results suggest that IGF-I stimulates the expression of AR coactivators by cooperative activation of the p38 MAPK and ERK1/2 pathways in C2C12 mouse skeletal muscle cells.

• Journal of Life Science
• /
• v.28 no.2
• /
• pp.265-273
• /
• 2018

Estrogen (E2) is involved in the development and progression of breast cancer and is mediated by estrogen receptor (ER). ER plays important roles in cellular proliferation, migration, invasion and causing drug resistance through diverse cross-talks with epidermal growth factor receptor (EGFR) and insulin-like growth factor-1 receptor (IGF-1R) signaling pathways in breast cancer cells. Breast cancer is caused mainly by break-down of homeostasis of endocrine signaling pathways especially by the uncontrolled expression and increased activities of E2/IGF-1/EGF, ER/G-protein estrogen receptor (GPER)/IGF-1R/EGFR and their intracellular signaling mediators. These changes influence the complex cross-talk between E2 and growth factors' signaling, eventually resulting in the progression of cancer and resistance against endocrine regulators. Thus, elucidation of the molecular mechanisms in stepwise of the cross-talk between E2 and growth factors will contribute to the customized treatment according to the diverse types of breast cancer. In particular, as strategies for the treatment of breast cancer with diverse genotypes and phenotypes, there can be use of aromatase inhibitors and blockers of E2 action for the ER+ hormone-dependent breast cancer cells and use of IGF-1R/EGFR activity blockers for suppression of cancer cell proliferation from the cross-talk between E2 and growth factors. Furthermore, changes in the expression of the ECM molecules regulated by the cross-talk between ER and EGFR/IGF-1R can be used for the targeted therapeutics against the migration of breast cancer cells. Therefore, it is required for the cross-talk among the signaling pathways of ER, GPER, IGF-1R and EGFR concerning cancer progression to be elucidated in more detail at the molecular level.

• Journal of Dairy Science and Biotechnology
• /
• v.34 no.1
• /
• pp.1-7
• /
• 2016

Colostrum, a nutrient-rich fluid produced by female mammals after giving birth, is the specific initial diet of mammalian neonates. Colostrum is important for the nutrition, growth, and development of newborn infants and contributes to the immunologic defense of neonates. It contains immunoglobulins, antimicrobial peptides, such as lactoferrin and lactoperoxidase, and other bioactive molecules, including growth factors, such as IGF (insulin-like growth factor), EGF (epithermal growth factor), $TGF-{\beta}$ (transforming growth factor), and FGF (fibroblast growth factor). Bovine colostrum is a rich source of growth factors, which play a central role in wound healing. The biological activities of colostrum emphasize the relevance of the synergistic activity of growth factors to stimulate keratinocyte proliferation and migration, which are essential for tissue repair. Colostrum increases the expression of early differentiation markers, such as keratin 1 and 10 and involucrin, and late differentiation markers, including loricrin and filaggrin. Additionally, colostrum increases granulation tissue volume in the dermis, suggesting that it has a beneficial effect on wound healing. The therapeutic use of colostrum or individual peptides present in colostrum has a positive and curative influence on various gastrointestinal diseases.

• The korean journal of orthodontics
• /
• v.27 no.6 s.65
• /
• pp.955-961
• /
• 1997

Nicotine is one of the major components of cigarette smoking which causes various systemic and local diseases to human body. Mitogenic effects of nicotine to systemic disease are interesting factors in the results of cellular Proliferation especially to vascular and pulmonary tissue or cells. The study of local effects concerns with destruction of tissue and delayed healing rate after various surgical treatment. Platelet-Derived Growth factor(PDGF) and Insulin-like growth factor(IGF) are blown as major mitogens to human PDL cells. The purpose of this study was to investgate the mitogenic effects of nicotine to human PDL cells. We studied the expression of PDGF-$\alpha$ receptor, PDGF-$\beta$receptor, and IGF-l receptor mRNA from the nicotine treated human PDL cells by northern analysis. The experimental groups were divided into different serum($1\%,\;10\%$) and nicotine (100ng/m1,1000ng/m1) concentrations and each group was studied by time course. The results of this study showed upregulation of PDGF-${\alpha},\;{\beta}$ receptor and IGF-l receptor mRNA at 100ng/ml nicotine concentration and $10\%$ serum group to the time course. These results suggest that physiologically attainable nicotine concentrations may stimulate the mitogenic gene synthesis to human PDL cells in vitro.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.45 no.6
• /
• pp.903-910
• /
• 2016

In this study, the expression level of estrogen receptor in an ovariectomized rat model was effectively enhanced by MS-10, Cirsium japonicum and Thymus vulgaris extract complex, in a reversible manner. MS-10 plays a positive role in enhancing estrogen activity at low concentrations, leading to improved women's health. In order to determine whether or not MS-10 improves menopausal symptoms clinically, a randomized, double-blinded, and placebo-controlled clinical study was carried out on 62 middle-aged women treated with 500 mg of MS-10 or placebo daily for 12 weeks. Clinical menopausal symptoms were evaluated by Kupperman's index (KI) detecting various menopausal symptoms, including hot flushes, parenthesis, insomnia, nervousness, melancholia, dizziness, fatigue, rheumatic pain, palpitations, formication, and headaches. Total KI score decreased significantly by about 18% upon ingestion of MS-10. Colpoxerosis, a main symptom of menopause, was significantly reduced by about 21% upon ingestion of MS-10 in contrast to placebo. In addition, reduction of insulin-like growth factor-1 with age was improved by over 10% upon ingestion of MS-10, whereas there were no significant difference with placebo. No side effects appeared after treatment with MS-10. Thus, MS-10 can be suggested as a plausible natural substance for improving women's health.

• Tuberculosis and Respiratory Diseases
• /
• v.58 no.4
• /
• pp.359-366
• /
• 2005

Background : IGFBP-3 inhibits the mitogenic and anti-apoptotic activity of IGF by blocking the binding of IGF to its receptor. However, under certain circumstances, IGFBP-3 can enhance the activity of IGF by protecting IGF from its degradation. More than half of the interindividual variations in IGFBP-3 levels are known to be genetically determined by the polymorphism at -202 locus of IGFBP-3 gene. Method : We attempted to ascertain whether A-202C polymorphic variation of IGFBP-3 gene constitutes a risk factor for non-small cell lung cancer (NSCLC), using PCR-restriction fragment length polymorphism (RFLP). Our study included 104 NSCLC patients and 104 age-, gender-, and smoking status-matched control subjects. Result : In the 104 NSCLC subjects, the genotypic frequencies at the -202 site were as follows: AA = 67 (64.4%), AC = 35 (33.7%), and CC = 2 (1.9%). We did detect significant differences in the genotypic distribution between the NSCLC and the control subjects (p<0.05), and the NSCLC risk correlated significantly with AA genotype at the -202 locus (AA>AC>CC). Using CC genotype as a reference, the odds ratio (OR) for the subjects with AC genotype was 2.60 (95% CI: 0.89 - 8.60), and the OR associated with AA genotype was 5.89 (95% CI: 1.92 - 21.16). Conclusion : These results indicate that the dysregulation of IGF axis should now be considered as another important risk factor for NSCLC, and a potential target for novel antineoplastic therapies and/or preventative strategies in high-risk groups.

• Journal of Life Science
• /
• v.13 no.4
• /
• pp.541-550
• /
• 2003

E2 glycoprotein of hepatitis C virus (HCV) comprises a surface of viral particle together with E1 glycoprotein, and is thought to be involved in the attachment of HCV viral particle to receptor (s) on the permissible cells including hepatocytes, B cells, T cells, and monocytes. We constructed a phage library expressing cellular proteins of hepatocytes on the phage surface, which turned out to be 8.8${\times}$$10^5$ cfu of diversity and carried inserts in 95% of library. We screened both cDNA phage library and 12-mer peptide library to identify the cellular proteins binding to E2 protein. Some intracellular proteins including tensin and membrane band 4.1 which are involved in signal transduction of survival and cytoskeleton organization, were selected from cDNA phage library through several rounds of panning and screening. On the contrary, membrane proteins such as CCR7, CKR-L2, and insulin-like growth factor-1 receptor were identified through screening of peptide library. Phages expressing peptides corresponding to those membrane proteins were bound to E2 protein specifically as determined by neutralization of binding assay. Since it is well known that HCV can infect T cells as well as hepatocytes, we examined to see if E2 protein can bind to CCR7, a member of C-protein coupled receptor family expressed on T cells, using CCR7 transfected tells. Human CCR7 cDNA was cloned into pcDNA3.1(-) vector and transfected into human embryonic kidney cell, 293T, and expressed on the surface of the cell as shown by flow cytometer. Binding assay of E2 protein using CCR7 transfected cells indicated that E2 protein bound to CCR7 by dose-dependent mode, giving rise to the possibility that CCR7 might be a putative cellular receptor for HCV.