Linc00152 promotes proliferation in gastric cancer through the EGFR-dependent pathway.
Linc00152 promotes proliferation in gastric cancer through the EGFR-dependent pathway.
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DOI：
10.1186/s13046-015-0250-6
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发表时间：
2015-11-04
期刊：
影响因子：
--
通讯作者：
Xu Z
中科院分区：
文献类型：
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作者：
Zhou J;Zhi X;Wang L;Wang W;Li Z;Tang J;Wang J;Zhang Q;Xu Z
Linc 00152与胃癌的发生、发展密切相关，但其具体作用机制尚不清楚。采用RT-PCR和Western blot检测Linc 00152和EGFR的表达。采用CCK-8法和EDU法检测BALB/C裸鼠异种移植过程中细胞增殖情况。通过RNA pull-down和RNA免疫沉淀法研究lncRNA与靶蛋白的相互作用。在本研究中，我们首次证实了72对胃癌患者组织中的细胞质表达的Linc 00152上调。Linc 00152 shRNA处理的MGC 803和HGC-27细胞的细胞增殖和肿瘤生长受到抑制。RNA pull-down和RIP实验表明Linc 00152可与EGFR直接结合，从而激活PI 3 K/AKT信号通路。我们首次发现Linc 00152可以通过EGFR介导的PI 3 K/AKT通路促进肿瘤生长，这可能是未来治疗的潜在靶点。
Linc00152 has been identified highly associated with the tumorigenesis and development of gastric cancer, however, the detailed mechanism of Linc00152 involved still remains unclear. RT-PCR and western blot were used to detect the expression of Linc00152 and EGFR. The CCK8 and EDU assay was employed to measure cell proliferation while xenotransplantation technology was applied in BALB/C nude mice. The interaction between lncRNA and target protein was investigated by RNA pull-down and RNA immunoprecipitation assay. In this study, we first confirmed the upregulation of cytoplasmic expressed Linc00152 in 72 pair tissues of gastric patients. A suppression of cell proliferation and tumor growth was obtained in MGC803 and HGC-27 cells treated with Linc00152 shRNA. RNA pull-down and RIP assay revealed that Linc00152 could directly bind with EGFR which caused an activation of PI3K/AKT signaling. We first found that Linc00152 could promote tumor growth through EGFR-mediated PI3K/AKT pathway which may serve as potential targets for therapy in the future.