Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2113279 | Cancer Letters | 2012 | 12 Pages |
Abstract
Mammalian target of rapamycin complex 1 (mTORC1) is frequently activated in human cancers; however, clinical trials of rapalog (the mTORC1 inhibitors) have shown that pancreatic ductal adenocarcinomas (PDACs) resist to the treatment. Rapalog treatment activated the extracellular signal-regulated kinase (ERK) pathway in K-Ras mt PDAC cells. K-Ras knockdown abolished the insulin-like growth factor-1 (IGF-1)-induced ERK pathway in the K-Ras mt PDAC cells and enhanced the therapeutic efficacy of everolimus in treating K-Ras mt PDAC cells-derived mouse xenografts. The results indicate that targeting of K-Ras mutation may lead to the development of therapies that overcome rapalog resistance in PDAC.
Keywords
Related Topics
Life Sciences
Biochemistry, Genetics and Molecular Biology
Cancer Research
Authors
Feng Wei, Yan Liu, Anita C. Bellail, Jeffrey J. Olson, Shi-Yong Sun, Guoyue Lu, Lijuan Ding, Changji Yuan, Guangyi Wang, Chunhai Hao,