根據衛生署在2010年的統計，口腔癌位居台灣人癌症十大死因第六名。先前研究顯示，許多癌症中都有被報導具有動情激素之過度表現，其中包含口腔癌。在人類鱗狀細胞癌組織和細胞株中，都觀察到有ERα 和ERβ不同的表現情形。G-protein-coupled receptor 30 (GPR30)，屬於rhodopsin-like receptor中的一類，為穿膜分子，且被發現能傳達動情素的許多細胞反應。文獻中指出，G15為GPR30抑制劑，可與GPR30結合，兩者具有高度的親和性，且在經由GPR30傳遞的動情素訊息路徑中扮演一個拮抗劑的角色。以SCC4、HSC3及SCC9人類口腔癌細胞株評估G15的體外活性中，G15會降低SCC4、HSC3及SCC9之細胞存活率且IC50值分別為11.2、7.8及15.6 μM。隨著藥物劑量的增加，在10 μΜ時，G15可使細胞週期明顯停滯在G2/M 期，在15 μΜ時，會誘發細胞凋亡，且caspase-3與caspase-9活化也支持這個結果。機制證據顯示G15負面調控CDK6、Cdc2、Cdc25C和NF-κB之表現。
In Taiwan, the oral cancer is situated sixth in the cancer causes of death, according to the department of health's statistics in 2010. In the previous reports, many cancers demonstrated the overexpression of estrogen receptors including oral cancer. Different expression patterns for ERα and ERβ were observed both in human Squamous cell carcinoma tissues (SCC) and cultured SCC cells. G-protein-coupled receptor (GPR30) belongs to rhodopsin-like receptor superfamily which is a transmembrane molecule that has been found to mediate several rapid cellular effects of estrogen. G15, a GPR30 inhibitor. It binds to GPR30 with high affinity and acts as an antagonist of estrogen signaling through GPR30. The in vitro effects of G15 were evaluated in SCC4, HSC3, and SCC9 human oral cancer cell lines, G15 reduced cell viability of SCC4, HSC3, and SCC9 cells with IC50 of 11.2, 7.8, and 15.6 μM, respectively. It induced G2/M arrest in a dose dependent manner up to 10 μM, and apoptosis at 15 μM, as evidenced by caspase-3 and caspase-9 activation. Mechanistic evidence indicates that G15 downregulated the expression of CDK6, Cdc2, Cdc25C and NF-κB.
