Department of Obstetrics and Gynecology, Center for Molecular Medicine, School of Medicine, Jichi Medical University, Tochigi, Japan.
Oncol Rep. 2012 May;27(5):1336-40. doi: 10.3892/or.2012.1626. Epub 2012 Jan 11.
The purpose of this study was to explore the possibility of targeted molecular therapy with anti-epidermal growth factor receptor (anti-EGFR) antibody (cetuximab) for the treatment of mucinous ovarian carcinoma. We analyzed EGFR protein expression and KRAS gene mutations in 5 mucinous ovarian carcinoma cell lines RMUG-L, RMUG-S, MN-1, OMC-1 and MCAS and evaluated the in vitro and in vivo effects of cetuximab on each. EGFR expression was observed in all cell lines except for MN-1 cells, and a KRAS gene mutation at codon 12 was detected only in the MCAS cell line. Cetuximab inhibited RMUG-L and OMC-1 cell growth in vitro and completely blocked RMUG-L tumor growth in vivo. On the other hand, cetuximab did not affect MCAS cell growth in vitro and only partially reduced the MCAS tumor growth in vivo. These results suggest the possibility of targeted molecular therapy with cetuximab for mucinous ovarian carcinoma cells lacking a KRAS gene mutation.
本研究旨在探讨表皮生长因子受体（anti-EGFR）抗体（西妥昔单抗）靶向分子治疗黏液性卵巢癌的可能性。我们分析了 5 株黏液性卵巢癌细胞系 RMUG-L、RMUG-S、MN-1、OMC-1 和 MCAS 中 EGFR 蛋白表达和 KRAS 基因突变，并评估了西妥昔单抗对每种细胞系的体外和体内作用。除 MN-1 细胞外，所有细胞系均观察到 EGFR 表达，仅在 MCAS 细胞系中检测到 KRAS 基因 12 密码子突变。西妥昔单抗抑制 RMUG-L 和 OMC-1 细胞的体外生长，并完全阻断 RMUG-L 肿瘤的体内生长。另一方面，西妥昔单抗对 MCAS 细胞的体外生长没有影响，仅部分减少 MCAS 肿瘤的体内生长。这些结果提示，对于缺乏 KRAS 基因突变的黏液性卵巢癌细胞，西妥昔单抗靶向分子治疗具有可能性。
