HRAS as a potential therapeutic target of salirasib RAS inhibitor in bladder cancer
HRAS as a potential therapeutic target of salirasib RAS inhibitor in bladder cancer
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DOI：
10.3892/ijo.2018.4435
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发表时间：
2018-08-01
影响因子：
5.2
通讯作者：
Nakagawa, Masayuki
中科院分区：
文献类型：
--
作者：
Sugita, Satoshi;Enokida, Hideki;Nakagawa, Masayuki
活性形式的小GT-RAS与下游效应物结合以促进细胞生长和增殖。RAS信号增强有助于各种不同癌症的肿瘤发生、侵袭和转移。HRAS原癌基因GT3（HRAS）是RAS亚型之一，是1982年在T24膀胱癌（BC）细胞中报道的第一个突变的人类癌基因，并且已经在几种癌症中报道了HRAS突变或上调。根据来自癌症基因组图谱的数据，与健康样品相比，临床BC样品中HRAS表达显著上调（P=0.0024）。HRAS基因突变的乳腺癌患者HRAS表达也显著高于无HRAS基因突变的乳腺癌患者（P
The active form of the small GTPase RAS binds to downstream effectors to promote cell growth and proliferation. RAS signal enhancement contributes to tumorigenesis, invasion, and metastasis in various different cancers. HRAS proto-oncogene GTPase (HRAS), one of the RAS isoforms, was the first human oncogene for which mutations were reported in T24 bladder cancer (BC) cells in 1982, and HRAS mutation or upregulation has been reported in several cancers. According to data from The Cancer Genome Atlas, HRAS expression was significantly upregulated in clinical BC samples compared to healthy samples (P=0.0024). HRAS expression was also significantly upregulated in BC with HRAS mutation compared to patients without HRAS mutation (P