Expression and regulation of the insulin-like growth factor-1 receptor by growing and quiescent H4IIE hepatoma
| Autor: | Lorraine Yau, Julieta Werner, Peter Zahradka |
|---|---|
| Rok vydání: | 1998 |
| Předmět: |
medicine.medical_treatment
Receptor expression Biophysics Biochemistry Receptor IGF Type 1 03 medical and health sciences Insulin-like growth factor Liver Neoplasms Experimental 0302 clinical medicine Tumor Cells Cultured medicine Animals Hypoglycemic Agents Insulin Insulin-Like Growth Factor I Receptor 030304 developmental biology Insulin-like growth factor 1 receptor Hepatoma 0303 health sciences biology Cell growth Cell Biology Molecular biology IRS2 Rats Gene Expression Regulation Neoplastic Insulin receptor Insulin-like growth factor-1 030220 oncology & carcinogenesis biology.protein Cell Division |
| Zdroj: | Biochimica et Biophysica Acta (BBA) - Biomembranes. 1375:131-139 |
| ISSN: | 0005-2736 |
| DOI: | 10.1016/s0005-2736(98)00144-8 |
| Popis: | Recent evidence that insulin-like growth factor-1 (IGF-1) influences certain properties of H4IIE hepatoma cells independent of insulin led us to examine whether H4IIE cells express IGF-1 receptors. Competitive binding experiments demonstrated IGF-1, but not insulin or IGF-II, could compete with [125I]IGF-1. Chemical crosslinking detected a protein with an apparent mass of 175 kDa and its identity as the IGF-1 receptor α-subunit was confirmed by Western blotting. The apparent molecular mass of this protein decreased to 135 kDa following deglycosylation. Immunofluorescence microscopy verified that both insulin and IGF-1 receptors were present, although measurement of IGF-1 receptor quantity revealed they were less abundant than insulin receptors. Binding of IGF-1 was low in growing cells and higher in a quiescent cell population. Scatchard analysis confirmed that receptor density was increased in non-growing H4IIE cells while there was no apparent difference in receptor affinity. Western blot analysis and RT-PCR revealed that both protein and mRNA levels were elevated as cell growth ceased. Interestingly, addition of insulin to quiescent H4IIE cells, which stimulates cell proliferation, further increased IGF-1 receptor protein levels with a peak at 12–24 h. Distinct modes of regulating IGF-1 receptor expression are indicated. |
| Databáze: | OpenAIRE |
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