Ras及其超家族成员Rho在人类肿瘤常因突变而异常激活，且与肿瘤发生和演进密切相关。鼻咽癌中虽常见Ras与Rho的持续激活，但其基因突变却很罕见，推测Ras负调控因子失活可能是鼻咽癌中Ras及Rho信号通路激活的重要原因。为寻找Ras的负调节因子，我们通过分析前期工作中高通量甲基化测序建立的鼻咽癌甲基化谱式，发现鼻咽癌中ARHGAP20基因可能因DNA高甲基化转录失活。ARHGAP20基因同时具有Ras相关和RhoGAP结构域，推测其可能同时或分别抑制Ras与Rho信号通路，从细胞增殖和转移两方面抑制肿瘤的恶性生物学行为，可能是一个新的强效抑癌基因。因此，本研究拟进一步在鼻咽癌组织中验证ARHGAP20基因的转录和表达失活及其机制和潜在的功能后果，探究ARHGAP20基因对Ras与Rho信号通路的调控及其影响鼻咽癌细胞增殖和转移行为的关分子机制，为深入了解鼻咽癌的发病机制提供基础数据。

Abnormal activation of Ras and Rho signaling by mutation is closely related to the tumorigenesis. In nasopharyngeal carcinoma (NPC), the activation of Ras and Rho is common, but the mutation is rare. Therefore, the inactivation of their negative regulators might be one of the main reasons. In previous study, we established a methylation profiles in NPC and found that ARHGAP20 is possibly inactivated by DNA hypermethylation. We hypothesis that ARHGAP20 could be a potent tumor suppressor gene, inhibiting tumor proliferation and metastasis as a potential negative regulator of Ras and Rho, due to containing both Ras associated domain and RhoGAP domains. Here, we aim to further verify the epigenetic inactivation of ARHGAP20 in NPC, to study the regulation of Ras and Rho signaling by ARHGAP20, to investigate the role of ARHGAP20 in the proliferation and metastasis of NPC cells, and the molecular mechanisms involved. Our results will provide scientific data for better understanding the pathogenesis of NPC.