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vilip-1 downregulation in non-small cell lung carcinomas mechanisms and prediction of survival在非小细胞肺癌癌差别vilip-1对这些基因的生存机制和预测
VILIP-1 Downregulation in Non-Small Cell Lung
Carcinomas: Mechanisms and Prediction of Survival
1 1 2 3 4 1 1
Jian Fu , Kathryn Fong , Alfonso Bellacosa , Eric Ross , Sinoula Apostolou , Daniel E. Bassi , Fang Jin ,
1 5 ˜ 5 6
Jirong Zhang , Paul Cairns , Inmaculada Ibanez de Caceres , Karl-Heinz Braunewell , Andres J. Klein-
Szanto1*
1 Department of Pathology, Fox Chase Cancer Center, Philadelphia, Pennsylvania, United States of America, 2 Human Genetics Program, Fox Chase Cancer Center,
Philadelphia, Pennsylvania, United States of America, 3 Biomathematics and Biostatistics, Fox Chase Cancer Center, Philadelphia, Pennsylvania, United States of America,
4 Bioinformatics Facility, Fox Chase Cancer Center, Philadelphia, Pennsylvania, United States of America, 5 Surgical Oncology, Fox Chase Cancer Center, Philadelphia,
´
Pennsylvania, United States of America, 6 Neuroscience Research Center of the Charite, Faculty of Medicine, Humboldt University, Berlin, Germany
Abstract
VILIP-1, a member of the neuronal Ca++ sensor protein family, acts as a tumor suppressor gene in an experimental animal
model by inhibiting cell proliferation, adhesion and invasiveness of squamous cell carcinoma cells. Western Blot analysis of
human tumor cells showed that VILIP-1 expression was undetectable in several types of human tumor cells, including 11 out
of 12 non-small cell lung carcinoma (NSCLC) cell lines. The down-regulation of VILIP-1 was due to loss of VILIP-1 mRNA
transcripts. Rearrangements, large gene deletions or mu
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