Department of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, Kyoto 606-8507, Japan.
Mol Cancer Ther. 2011 Apr;10(4):580-90. doi: 10.1158/1535-7163.MCT-10-0763. Epub 2011 Jan 31.
Invasion into deep myometrium and/or lymphovascular space is a well-known risk factor for endometrial cancer metastasis, resulting in poor prognosis. It is therefore clinically important to identify novel molecules that suppress tumor invasion. Reduced expression of the metastasis suppressor, kisspeptin (KISS1), and its endogenous receptor, GPR54, has been reported in several cancers, but the significance of the KISS1/GPR54 axis in endometrial cancer metastasis has not been clarified. Metastin-10 is the minimal bioactive sequence of genetic products of KISS1. Clinicopathological analysis of 92 endometrial cancers revealed overall survival is improved in cancers with high expression of GPR54 (P < 0.05) and that GPR54 expression is associated with known prognostic factors including FIGO stage, grade, and deep myometrial invasion. Through RNAi and microarray analyses, metastin-10 was predicted to suppress metastasis of GPR54-expressing endometrial cancers in vivo. Methylation analysis revealed GPR54 is epigenetically regulated. Metastin-GPR54 axis function was restored following treatment with the DNA hypomethylating agent 5-aza-DC. These data suggest that metastin-10 may be effective at inhibiting the metastatic spread of endometrial cancers in combination with demethylating agents to induce GPR54 expression.
浸润至深肌层和/或淋巴管是子宫内膜癌转移的一个众所周知的危险因素,导致预后不良。因此,临床上重要的是要识别出能抑制肿瘤侵袭的新型分子。在几种癌症中,已报道有转移抑制因子 kisspeptin(KISS1)及其内源性受体 GPR54 的表达减少,但 KISS1/GPR54 轴在子宫内膜癌转移中的意义尚未阐明。Metastin-10 是 KISS1 基因产物的最小生物活性序列。对 92 例子宫内膜癌的临床病理分析显示,GPR54 高表达的癌症患者总体生存率提高(P<0.05),GPR54 表达与包括 FIGO 分期、分级和深肌层浸润在内的已知预后因素相关。通过 RNAi 和微阵列分析,预测 metastin-10 可抑制体内表达 GPR54 的子宫内膜癌的转移。甲基化分析显示 GPR54 受到表观遗传调控。用 DNA 去甲基化剂 5-aza-DC 处理后,恢复了 metastin-GPR54 轴的功能。这些数据表明,metastin-10 可能与去甲基化剂联合使用,通过诱导 GPR54 表达,有效抑制子宫内膜癌的转移扩散。