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Inhibition of RPS6K reveals context-dependent Akt activity in luminal breast cancer cells
Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology. Department of Computational & Systems Biology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America; University of Pittsburgh Drug Discovery Institute (UPDDI), University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.ORCID iD: 0000-0003-3663-3646
2021 (English)In: PloS Computational Biology, ISSN 1553-734X, E-ISSN 1553-7358, Vol. 17, no 6, article id e1009125Article in journal (Refereed) Published
Abstract [en]

Aberrant signaling through insulin (Ins) and insulin-like growth factor I (IGF1) receptors contribute to the risk and advancement of many cancer types by activating cell survival cascades. Similarities between these pathways have thus far prevented the development of pharmacological interventions that specifically target either Ins or IGF1 signaling. To identify differences in early Ins and IGF1 signaling mechanisms, we developed a dual receptor (IGF1R & InsR) computational response model. The model suggested that ribosomal protein S6 kinase (RPS6K) plays a critical role in regulating MAPK and Akt activation levels in response to Ins and IGF1 stimulation. As predicted, perturbing RPS6K kinase activity led to an increased Akt activation with Ins stimulation compared to IGF1 stimulation. Being able to discern differential downstream signaling, we can explore improved anti-IGF1R cancer therapies by eliminating the emergence of compensation mechanisms without disrupting InsR signaling.

Place, publisher, year, edition, pages
Public Library of Science (PLoS), 2021. Vol. 17, no 6, article id e1009125
National Category
Bioinformatics and Systems Biology
Identifiers
URN: urn:nbn:se:umu:diva-218250DOI: 10.1371/journal.pcbi.1009125ISI: 000670619100002PubMedID: 34191793OAI: oai:DiVA.org:umu-218250DiVA, id: diva2:1820883
Funder
NIH (National Institutes of Health), P30 CA047904NIH (National Institutes of Health), U01CA204826Available from: 2023-12-19 Created: 2023-12-19 Last updated: 2024-04-16Bibliographically approved

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Erdem, Cemal

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