@article{oai:repo.qst.go.jp:00045776,
 author = {Sudou, Hitomi and Tsuji, Atsushi and Sugyou, Aya and Sogawa, Chizuru and Yoshida, Chisato and Harada, Yoshinobu and Hino, Okio and Saga, Tsuneo and et.al and 須藤 仁美 and 辻 厚至 and 須尭 綾 and 曽川 千鶴 and 吉田 千里 and 原田 良信 and 佐賀 恒夫},
 issue = {4},
 journal = {Genomics},
 month = {Feb},
 note = {Malignant mesothelioma is a highly aggressive tumor arising from serosal surfaces of the pleura and is triggered by past exposure to asbestos. Currently, there is no widely accepted treatment for mesothelioma. Development of effective drug treatments for human cancers requires identification of therapeutic molecular targets. We therefore conducted a large-scale functional screening of mesothelioma cells using a genome-wide small interfering RNA library. We determined that knockdown of 39 genes suppressed mesothelioma cell proliferation. At least seven of the 39 genes—COPA, COPB2, EIF3D, POLR2A, PSMA6, RBM8A, and RPL18A—would be involved in anti-apoptotic function. In particular, the COPA protein was highly expressed in some mesothelioma cell lines but not in a pleural mesothelial cell line. COPA knockdown induced apoptosis and suppressed tumor growth in a mesothelioma mouse model. Therefore, COPA may have the potential of a therapeutic target and a new diagnostic marker of mesothelioma.},
 pages = {210--216},
 title = {Knockdown of COPA, Identified by Loss-of-Function Screen, Induces  Apoptosis and Suppresses Tumor Growth in Mesothelioma Mouse Model},
 volume = {95},
 year = {2010}
}