ArticleThe Journal of biological chemistry2010
Selective disruption of insulin-like growth factor-1 (IGF-1) signaling via phosphoinositide-dependent kinase-1 prevents the protective effect of IGF-1 on human cancer cell death.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 26 citations in OpenAlex.
- Dual role of PID1 in regulating apoptosis induced by distinct anticancer-agents through AKT/Raf-1-dependent pathway in hepatocellular carcinoma.Cell death discovery · 2023Article
- Combined targeting of MEK and the glucocorticoid receptor for the treatment of RAS-mutant multiple myeloma.BMC cancer · 2020Article
- Mammary Adipose Tissue Control of Breast Cancer Progression: Impact of Obesity and Diabetes.Frontiers in oncology · 2020Review
- IGF1R upregulation confers resistance to isoform-specific inhibitors of PI3K in PIK3CA-driven ovarian cancer.Cell death & disease · 2018Article
- IGF1/IGF1R and microRNA let-7e down-regulate each other and modulate proliferation and migration of colorectal cancer cells.Cell cycle (Georgetown, Tex.) · 2018Article
- Pathophysiological mechanisms of death resistance in colorectal carcinoma.World journal of gastroenterology · 2015Review
- Platelet-Rich Plasma Increases Growth and Motility of Adipose Tissue-Derived Mesenchymal Stem Cells and Controls Adipocyte Secretory Function.Journal of cellular biochemistry · 2015Article
- PPARG in Human Adipogenesis: Differential Contribution of Canonical Transcripts and Dominant Negative Isoforms.PPAR research · 2014Article
- MicroRNA-497 targets insulin-like growth factor 1 receptor and has a tumour suppressive role in human colorectal cancer.Oncogene · 2013Article
- Adipocyte-released insulin-like growth factor-1 is regulated by glucose and fatty acids and controls breast cancer cell growth in vitro.Diabetologia · 2012Article
- Insulin-like growth factor receptor-1 and nuclear factor κB are crucial survival signals that regulate caspase-3-mediated lens epithelial cell differentiation initiation.The Journal of biological chemistry · 2012Article
- Article
- Differential expression of TNF-α signaling molecules and ERK1 in distal and proximal colonic tumors associated with obesity.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2011Article
- Dual targeting of the insulin-like growth factor and collateral pathways in cancer: combating drug resistance.Cancers · 2011Article
- Defining the pathway to insulin-like growth factor system targeting in cancer.Biochemical pharmacology · 2010Review
- PDK1 recruitment to the SHPS-1 signaling complex enhances insulin-like growth factor-i-stimulated AKT activation and vascular smooth muscle cell survival.The Journal of biological chemistry · 2010Article
- Molecular signaling involving intrinsically disordered proteins in prostate cancer.Asian journal of andrologyReview
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
Insulin-like growth factor-1 (IGF-1) signaling system exerts a broad antiapoptotic function and plays a crucial role in resistance to anticancer therapies. Exposure of MCF-7 breast cancer cells to IGF-1 rapidly and transiently induced tyrosine phosphorylation and activation of phosphoinositide-dependent kinase-1 (PDK1). This was paralleled by Akt/protein kinase B and protein kinase C-zeta phosphorylation, at Thr(308) and Thr(410), respectively. IGF-1 treatment also enhanced PDK1 interaction with IGF-1 receptor (IGF-1R) in intact MCF-7 cells. Pulldown assays revealed that PDK1 bound IGF-1R in vitro and that the region encompassing amino acids 51-359 of PDK1 was necessary for the interaction. Synthetic peptides corresponding to IGF-1R C terminus amino acids 1295-1337 (C43) and to PDK1 amino acids 114-141 reduced in vitro IGF-1R/PDK1 interaction in a concentration-dependent manner. Loading of fluoresceinated-C43 (fluorescein isothiocyanate (FITC)-C43) into MCF-7 cells significantly reduced IGF-1R/PDK1 interaction and phosphorylation of PDK1 substrates. Moreover, FITC-C43 intracellular loading reverted the protective effect of IGF-1 on growth factor deprivation-induced cell death. Finally, the inhibition of IGF-1R/PDK1 interaction and signaling by FITC-C43 was accompanied by 2-fold enhanced killing capacity of cetuximab in human GEO colon adenocarcinoma cells and was sufficient to restore cell death in cetuximab-resistant cell clones. Thus, disruption of PDK1 interaction with IGF-1R reduces IGF-1 survival effects in cancer cells and may enhance cell death by anticancer agents.
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