Rapamycin induces feedback activation of Akt signaling through an IGF-1R-dependent mechanism

By X. Wan, B. Harkavy, N. Shen, P. Grohar, L. Helman. Oncogene, 2007

780 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/3b357bc0e3e9079e3c19e8f1dcc56cf8f4cf74c9

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In Immunology

In Molecular Biology

Citations in the corpus

An Integrative Genomic and Proteomic Analysis of PIK3CA, PTEN, and AKT Mutations in Breast Cancer (2008, background): “Whether mTOR represents a suboptimal target for therapy in breast cancer, whether other combinations of therapies with mTOR inhibition will be effective, or whether feedback loops bypass the activity of mTOR inhibitors requires additional analysis (22).”
The PTEN–PI3K pathway: of feedbacks and cross-talks (2008, background): “…negative feedback might be the most prominent mechanism leading to PI3K activation, other negative feedbacks have also been proposed. mTORC1 inhibition in rhabdomyosarcoma cells leads to AKT activation through a S6K–IRS-1independent signal that relies on IGF1R activation (Wan et al., 2007).”
Characterization of a naturally occurring breast cancer subset enriched in epithelial-to-mesenchymal transition and stem cell characteristics. (2009, background): “However, alterations in PI3K/AKT pathway activation by processes independent of mutations, by other interacting pathways, or by signaling modulation through feedback loops may have prevented identification of statistically significant associations (33).”
Active-Site Inhibitors of mTOR Target Rapamycin-Resistant Outputs of mTORC1 and mTORC2 (2009, background): “Rapamycin often stimulates the phosphorylation of Akt [47,48], probably by relieving feedback inhibition from S6K to the insulin receptor substrate 1 (IRS1) [49], a key signaling molecule that links activation of the insulin receptor to PI3K activation.”
Molecular biology in breast cancer: intrinsic subtypes and signaling pathways. (2012, background): “IGF pathway is regulated in many critical points, from ligand availability to negative feedback mechanisms exerted by mTOR.(67) As for its role in oncogenesis, preclinical studies show that the overexpression of IGF1R can induce the formation of tumors and facilitate metastasis formation.”
Defining the role of mTOR in cancer. (2007, background): “Dual inhibition of the PI3K pathway or other signaling pathways and mTOR could be an effective strategy (Fan and Weiss, 2006; Wan et al., 2007).”
Insulin receptor isoforms and insulin receptor/insulin-like growth factor receptor hybrids in physiology and disease. (2009, background): “Cell pretreatment with an IGF-IR blocking antibody (h7C10) (283) resulted in prevention of Akt activation and improved inhibition of rhabdomyosarcoma cell growth and survival.”