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首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >Inhibition of Myc effectively targets KRAS mutation-positive lung cancer expressing high levels of Myc.
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Inhibition of Myc effectively targets KRAS mutation-positive lung cancer expressing high levels of Myc.

机译：抑制Myc可有效靶向表达高水平Myc的KRAS突变阳性肺癌。

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摘要

Myc is an oncogenic transcription factor that promotes tumorigenesis. Recently, a dominant negative form of Myc (Omomyc) was shown to cause regression of lung tumors in a mouse model of lung cancer caused by KRAS mutation, suggesting that Myc might be a potential therapeutic target to treat the KRAS lung cancer. However, it is not yet known whether Omomyc can also inhibit the growth of human lung tumors that carry a similar KRAS mutation. In the present study, we demonstrate that Omomyc induces cell death of KRAS-mutated human lung adenocarcinoma A549 cells in vitro and in vivo. However, Omomyc does not induce cell death in human lung adenocarcinoma H441 cells that also carry the KRAS mutation. Interestingly, A549 cells express high levels of Myc, while H441 cells do not. Co-expression of exogenous Myc with Omomyc in H441 cells induces cell death, indicating that Omomyc requires high levels of Myc to induce cell death in KRAS mutation-positive lung adenocarcinoma. Here, we show for the first time that KRAS mutation-positive lung cancer displaying high levels of Myc could be treated by inhibiting Myc transactivation function.
机译：Myc是促进肿瘤发生的致癌转录因子。最近，显示出显性阴性形式的Myc（Omomyc）在由KRAS突变引起的肺癌小鼠模型中引起肺肿瘤消退，这表明Myc可能是治疗KRAS肺癌的潜在治疗靶标。但是，尚不知道Omomyc是否也能抑制带有类似KRAS突变的人肺肿瘤的生长。在本研究中，我们证明了Omomyc在体外和体内均可诱导KRAS突变的人肺腺癌A549细胞死亡。但是，Omomyc不会在同样带有KRAS突变的人肺腺癌H441细胞中诱导细胞死亡。有趣的是，A549细胞表达高水平的Myc，而H441细胞则不。外源性Myc与Omomyc在H441细胞中共表达可诱导细胞死亡，这表明Omomyc需要高水平的Myc才能诱导KRAS突变阳性的肺腺癌中的细胞死亡。在这里，我们首次证明可以通过抑制Myc反式激活功能来治疗高水平Myc的KRAS突变阳性肺癌。

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