@article{oai:ir.kagoshima-u.ac.jp:00001030,
 author = {Kunigou, Osamu and 救仁郷, 修 and Nagao, Hiroko and 永尾, 宗子 and Kawabata, Naoya and 川畑, 直也 and Ishidou, Yasuhiro and 石堂, 康弘 and Nagano, Satoshi and 永野, 聡 and Maeda, Shingo and 前田, 真吾 and Komiya, Setsuro and 小宮, 節郎 and Setoguchi, Takao and 瀬戸口, 啓夫},
 issue = {5},
 journal = {Oncology Reports},
 month = {},
 note = {GOLPH3 was originally identified by proteomic analyses of Golgi proteins localized in the trans-Golgi network. Recently, it was reported that GOLPH3 is up-regulated in various types of malignancies, including melanoma, colon cancer and lung cancer. However, the mechanism through which GOLPH3 is involved in the pathogenesis of rhabdomyosarcoma remains unidentified. In order to explore the function of GOLPH3 and its isoform, GOLPH3L, in the pathogenesis of rhabdomyosarcoma, we investigated the expression and knockdown effects of GOLPH3 and GOLPH3L in human rhabdomyosarcoma. Western blot analysis and real-time PCR revealed that human rhabdomyosarcoma cell lines and biopsy specimens exhibited an increased expression of GOLPH3 and GOLPH3L. GOLPH3 and GOLPH3L knockdown by siRNA prevented the proliferation of human rhabdomyosarcoma cell lines. In addition, double-knockdown of GOLPH3 and GOLPH3L also prevented the proliferation of rhabdomyosarcoma cell lines. Our findings improve the understanding of rhabdomyosarcoma pathogenesis and suggest that the knockdown of GOLPH3 or GOLPH3L may be an effective treatment for rhabdomyosarcoma.},
 pages = {1337--1442},
 title = {Role of GOLPH3 and GOLPH3L in the proliferation of human rhabdomyosarcoma},
 volume = {26},
 year = {2011},
 yomi = {クニゴウ, オサム and ナガオ, ヒロコ and カワバタ, ナオヤ and イシドウ, ヤスヒロ and ナガノ, サトシ and マエダ, シンゴ and コミヤ, セツロウ and セトグチ, タカオ}
}