Adenocarcinoma, a form of non-small cell lung cancer (NSCLC), is the most commonly diagnosed lung cancer subtype. It comprises some 40% of all diagnoses, and is the most common subtype afflicting women and non-smokers. The negative systemic effects of standard NSCLC chemotherapy and bleak five-year patient survival rates have pushed researchers to explore the use of more targeted treatment engineered towards specific oncogenic molecules. We propose that CAPER, a coactivator of AP-1 and estrogen receptor, could serve as a novel therapeutic target in adenocarcinoma. We found that CAPER was significantly upregulated in patient adenocarcinoma tissue in comparison to normal samples. Additionally, lentiviral-mediated knockdown of CAPER expression in human lung adenocarcinoma cell lines decreased cell number by 60% and significantly increased the survival of mice in an orthotopic xenograft model. This effect can be attributed to G2/M phase cell cycle arrest, the induction of apoptosis, and increased reactive oxygen species.
|School:||University of the Sciences in Philadelphia|
|Department:||Pharmacology and Toxicology|
|School Location:||United States -- Pennsylvania|
|Source:||MAI 57/05M(E), Masters Abstracts International|
|Subjects:||Pharmaceutical sciences, Oncology|
|Keywords:||Adenocarcinoma, Ap-1, Apoptosis, Caper, G2/m phase arrest, Nsclc|
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