Adenovirus vector-mediated FAM176A overexpression induces cell death in human H1299 non-small cell lung cancer cells.
Adenovirus vector-mediated FAM176A overexpression induces cell death in human H1299 non-small cell lung cancer cells.
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DOI：
10.5483/bmbrep.2014.47.2.090
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发表时间：
2014-02
期刊：
影响因子：
3.8
通讯作者：
Chen Y
中科院分区：
文献类型：
--
作者：
Xie H;Hu J;Pan H;Lou Y;Lv P;Chen Y
FAM176A(序列相似性176个成员A)是一个与细胞程序性死亡相关的新分子。FAM176A在包括肺癌在内的几种类型的人类肿瘤中的表达降低。在本研究中，我们研究了FAM176A对人非小细胞肺癌细胞系H1299细胞的生物活性。我们构建了重组腺病毒5-FAM176A载体(Ad5-FAM176A)，并对其表达和体外抗肿瘤活性进行了研究。细胞存活率分析显示，腺病毒介导的FAM176A的增加抑制了肿瘤细胞的生长，并呈剂量和时间依赖关系。这种抑制作用是通过自噬和涉及caspase激活的细胞凋亡来实现的。此外，细胞周期分析显示Ad5-FAM176A可诱导细胞周期停滞于G2/M期，提示腺病毒介导的FAM176A基因转移可能为肺癌的治疗提供新的途径。[BMB报告2014；47(2)：104-109]
FAM176A (family with sequence similarity 176 member A) is a novel molecule related to programmed cell death. A decreased expression of FAM176A has been found in several types of human tumors in including lung cancers. In the present study, we investigated the biological activities of FAM176A on the human non–small cell lung cancer cell line H1299 cells. We constructed a recombinant adenovirus 5-FAM176A vector (Ad5-FAM176A) and evaluated the expression and anti-tumor activities in vitro. Cell viability analysis revealed that the adenovirus-mediated increase of FAM176A inhibited the growth of the tumor cells in a dose- and time-dependent manner. This inhibitory effect was mediated by both autophagy and apoptosis that involved caspase activation. In addition, cell cycle analysis suggested that Ad5-FAM176A could induce cell cycle arrest at the G2/M phase, all of which suggested that adenovirus-mediated FAM176A gene transfer might present a new therapeutic approach for lung cancer treatment. [BMB Reports 2014; 47(2): 104-109]
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