The role of the Akt/mTOR pathway in tobacco carcinogen-induced lung tumorigenesis.
Lung cancer is the leading cause of cancer-related death in the United States, and 85 to 90% of lung cancer cases are associated with tobacco use. Tobacco components promote lung tumorigenesis through genotoxic effects, as well as through biochemical modulation of signaling pathways such as the Akt/mammalian target of rapamycin (mTOR) pathway that regulates cell proliferation and survival. This review will describe cell surface receptors and other upstream components required for tobacco carcinogen-induced activation of Akt and mTOR. Preclinical studies show that inhibitors of the Akt/mTOR pathway inhibit tumor formation in mouse models of carcinogen-induced lung tumorigenesis. Some of these inhibitors will be highlighted, and their clinical potential for the treatment and prevention of lung cancer will be discussed.
Duke Scholars
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Related Subject Headings
- TOR Serine-Threonine Kinases
- Smoking
- Sirolimus
- Signal Transduction
- Rotenone
- Proto-Oncogene Proteins c-akt
- Protein Serine-Threonine Kinases
- Oncology & Carcinogenesis
- Nicotiana
- Mice
Citation
Published In
DOI
EISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- TOR Serine-Threonine Kinases
- Smoking
- Sirolimus
- Signal Transduction
- Rotenone
- Proto-Oncogene Proteins c-akt
- Protein Serine-Threonine Kinases
- Oncology & Carcinogenesis
- Nicotiana
- Mice