Gene therapy of murine teratocarcinoma: separate functions for insulin-like growth factors I and II in immunogenicity and differentiation
| Autor: | S D Rudin, T R Johnson, B K Blossey, Mark L. Tykocinski, Fadi W. Abdul-Karim, J Trojan, Donald D. Anthony, Alexander Shevelev, Judith Ilan, K. M. Kelley |
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| Rok vydání: | 1994 |
| Předmět: |
Teratocarcinoma
Mesoderm Transcription Genetic medicine.medical_treatment Cellular differentiation Molecular Sequence Data Restriction Mapping Gene Expression Ectoderm Mice Inbred Strains Biology Transfection Immunoenzyme Techniques Mice Insulin-Like Growth Factor II medicine Tumor Cells Cultured Animals Insulin-Like Growth Factor I Receptor Multidisciplinary Base Sequence Growth factor Cell Differentiation Genetic Therapy Oligonucleotides Antisense Embryonic stem cell Molecular biology Immunohistochemistry Cell biology medicine.anatomical_structure embryonic structures Endoderm Research Article |
| Zdroj: | Proceedings of the National Academy of Sciences of the United States of America. 91(13) |
| ISSN: | 0027-8424 |
| Popis: | Teratocarcinoma is a germ-line carcinoma giving rise to an embryoid tumor with structures derived from the three embryonic layers: mesoderm, endoderm, and ectoderm. Teratocarcinoma is widely used as an in vitro model system to study regulation of cell determination and differentiation during mammalian embryogenesis. Murine embryonic carcinoma (EC) PCC3 cells express insulin-like growth factor I(IGF-I) and its receptor, while all derivative tumor structures express IGF-I and IGF-II and their receptors. Therefore the system lends itself to dissect the role of these two growth factors during EC differentiation. With an episomal antisense strategy, we define a role for IGF-I in tumorigenicity and evasion of immune surveillance. Antisense IGF-I EC transfectants are shown to elicit a curative anti-tumor immune response with tumor regression at distal sites. In contrast, IGF-II is shown to drive determination and differentiation in EC cells. Since IGF-I and IGF-II bind to type I receptor and antisense sequence used for IGF-II cannot form duplex with endogenous IGF-I transcripts, it follows that this receptor is not involved in determination and differentiation. |
| Databáze: | OpenAIRE |
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