Journal
TRENDS IN BIOCHEMICAL SCIENCES
Volume 38, Issue 12, Pages 612-620Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tibs.2013.10.001
Keywords
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
Categories
Funding
- Cancer Genomics Center
- Center for Biomedical Genetics
- Swedish Cancerfonden
- Key Construction Program of the National '985' Project
- Zhejiang University Special Fund for Fundamental Research
- Fundamental Research Funds for the Central Universities
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available
Share Paper
