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IGF1Ec expression in MG-63 human osteoblast-like osteosarcoma cells
Anastassios Philippou1, Athanasios Armakolas, Zacharoula Panteleakou
1Department of Experimental Physiology, Medical School, National & Kapodistrian University of Athens, 75 Micras Asias, Goudi-Athens 11527, Greece.
Anticancer Research
|December 27, 2011
Summary
The insulin-like growth factor 1 (IGF1) system
Area of Science:
- Molecular Biology
- Endocrinology
- Cancer Research
Background:
- The insulin-like growth factor 1 (IGF1) gene exhibits complex alternative splicing, producing multiple transcripts.
- Understanding IGF1 system expression and function is crucial in osteosarcoma biology.
Purpose of the Study:
- To investigate the expression and functional role of IGF1 isoforms in human MG-63 osteosarcoma cells.
- To elucidate the mechanisms of IGF1-mediated mitogenesis in these cells.
Main Methods:
- Reverse transcription polymerase chain reaction (RT-PCR) and quantitative real time-PCR (qRT-PCR) for transcript analysis.
- Western blot analysis for protein expression.
- Cell proliferation assays using MG-63 cells and genetically modified variants (IGF1R KO, INSR KO).
Main Results:
- MG-63 cells express IGF1Ea and IGF1Ec isoforms; dihydrotestosterone (DHT) upregulates these and induces IGF1Eb.
- IGF1, insulin, and a synthetic E peptide stimulate MG-63 cell growth.
- The synthetic E peptide promotes growth independently of IGF1 receptor (IGF1R) and insulin receptor (INSR).
Conclusions:
- IGF1 isoform expression in MG-63 cells is hormonally regulated.
- The IGF1Ec peptide may play a role in osteosarcoma progression through an IGF1R- and INSR-independent pathway.
