ArticleMolecular and cellular biology1997
Insulin-like growth factor I receptor signaling in transformation by src oncogenes.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 85 citations in OpenAlex.
- Novel Regulators of the IGF System in Cancer.Biomolecules · 2021Review
- The impact of the IGF-1 system of cancer cells on radiation response - AnClinical and translational radiation oncology · 2017Article
- Insulin/Insulin-like growth factors in cancer: new roles for the aryl hydrocarbon receptor, tumor resistance mechanisms, and new blocking strategies.Frontiers in endocrinology · 2015Review
- Growth of v-src-transformed cells in serum-free medium through the induction of growth factors.Journal of cellular physiology · 2013Article
- Targeting insulin-like growth factor axis in hepatocellular carcinoma.Journal of hematology & oncology · 2011Review
- The insulin receptor: a new target for cancer therapy.Frontiers in endocrinology · 2011Article
- IGF-I induced genes in stromal fibroblasts predict the clinical outcome of breast and lung cancer patients.BMC medicine · 2010Article
- Insulin-like growth factor-1 receptor-targeted therapy for non-small cell lung cancer: a mini review.American journal of translational research · 2009Article
- Transformation by the simian virus 40 T antigen is regulated by IGF-I receptor and IRS-1 signaling.Oncogene · 2006Article
- A high expression level of insulin-like growth factor I receptor is associated with increased expression of transcription factor Sp1 and regional lymph node metastasis of human gastric cancer.Clinical & experimental metastasis · 2004Article
- Coexpression of IGF-1R and c-Src proteins in human pancreatic ductal adenocarcinoma.Digestive diseases and sciences · 2003Article
- Molecular basis of angiogenesis and cancer.Oncogene · 2003Review
- Article
- Regulation of insulin-like growth factor type I (IGF-I) receptor kinase activity by protein tyrosine phosphatase 1B (PTP-1B) and enhanced IGF-I-mediated suppression of apoptosis and motility in PTP-1B-deficient fibroblasts.Molecular and cellular biology · 2002Article
- Activation of the IGF-IR system contributes to malignant growth of human and mouse medulloblastomas.Oncogene · 2001Article
- IGF-I receptor signalling in transformation and differentiation.Molecular pathology : MP · 2001Review
- Review
- Function of the IGF-I receptor in breast cancer.Journal of mammary gland biology and neoplasia · 2000Review
- Induction of tumor suppression and glandular differentiation of A549 lung carcinoma cells by dominant-negative IGF-I receptor.Oncogene · 1999Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
R- cells, a line of mouse embryo fibroblasts with a targeted disruption of the insulin-like growth factor I (IGF-I) receptor genes, are refractory to transformation by several viral and cellular oncogenes. Using colony formation in soft agar as a measure of full transformation, we report here that R- cells can be transformed by v-src, although they still cannot be transformed by the activated c-src527 (mutation at tyrosine 527 to phenylalanine), which readily transforms mouse embryo cells with a wild-type number of IGF-I receptors (W cells). Although v-src is a more potent inducer of tyrosine phosphorylation than c-src527, the extent of phosphorylation of either insulin receptor substrate 1 or Shc, two of the major substrates of the IGF-I receptor, does not seem sufficiently different to explain the qualitative difference in soft agar growth. v-src, however, is considerably more efficient than c-src527 in its ability to tyrosyl phosphorylate, in R- cells, the focal adhesion kinase, Stat1, and p130cas. These results indicate that v-src, but not c-src527, can bypass the requirement for a functional IGF-I receptor in the full transformation of mouse embryo fibroblasts and suggest that qualitative and quantitative differences between the two oncogenes can be used to identify some of the signals relevant to the mechanism(s) of transformation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.