Signaling interplay between transforming growth factor-beta receptor and PI3K/AKT pathways in cancer
2013 (English)In: TIBS -Trends in Biochemical Sciences. Regular ed., ISSN 0968-0004, Vol. 38, no 12, 612-620 p.Article, review/survey (Refereed) Published
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.
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
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:uu:diva-215454DOI: 10.1016/j.tibs.2013.10.001ISI: 000328590500004OAI: oai:DiVA.org:uu-215454DiVA: diva2:687338