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Signaling interplay between transforming growth factor-beta receptor and PI3K/AKT pathways in cancer
Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang 310058, China.
Department of Molecular Cell Biology, Cancer Genomics Centre and Centre for Biomedical Genetics, Leiden University Medical Center, Leiden, The Netherlands.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Ludwig Institute for Cancer Research. Department of Molecular Cell Biology, Cancer Genomics Centre and Centre for Biomedical Genetics, Leiden University Medical Center, Leiden, The Netherlands.
2013 (English)In: TIBS -Trends in Biochemical Sciences. Regular ed., ISSN 0968-0004, E-ISSN 1362-4326, Vol. 38, no 12, 612-620 p.Article, review/survey (Refereed) Published
Abstract [en]

The transforming growth factor (TGF)-beta and phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathways are used in cells to control numerous responses, including proliferation, apoptosis, and migration. TGF-beta is known for its cytostatic effect's in premalignant states and its pro-oncogenic activity in advanced cancers. The pro-cell survival response exerted by growth-factor-mediated activation of PI3K/AKT has been linked to stimulation of tumor formation. Both TGF-beta receptor and PI3K/AKT pathways were initially modeled as linear signaling conduits. Although early studies suggested that these two pathways might counteract each other in balancing cell survival, emerging evidence has uncovered multiple modes of intricate signal integration and obligate collaboration in driving cancer progression. These new insights provide the rationale for exploring their dual targeting in cancer.

Place, publisher, year, edition, pages
2013. Vol. 38, no 12, 612-620 p.
Keyword [en]
AKT, phosphoinositide 3-kinase, phosphatase and tensin homolog deleted on chromosome 10, SMA- and MAD-related protein (SMAD) transforming growth factor-beta, mammalian target of rapamycin complex
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Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-215454DOI: 10.1016/j.tibs.2013.10.001ISI: 000328590500004OAI: oai:DiVA.org:uu-215454DiVA: diva2:687338
Available from: 2014-01-14 Created: 2014-01-14 Last updated: 2017-12-06Bibliographically approved

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