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首页> 外文期刊>Lung cancer: Journal of the International Association for the Study of Lung Cancer >Apolipoprotein E expression promotes lung adenocarcinoma proliferation and migration and as a potential survival marker in lung cancer.
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Apolipoprotein E expression promotes lung adenocarcinoma proliferation and migration and as a potential survival marker in lung cancer.

机译:载脂蛋白E的表达促进了肺腺癌的增殖和迁移,并成为肺癌的潜在生存标志。

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摘要

Many human lung cancer cell lines express apolipoprotein E (ApoE), especially cells derived from malignant pleural effusions (MPE) in patients with lung adenocarcinoma. This study aimed to investigate the influence of ApoE expression on lung cancer. In lung cancer tissues, ApoE expression was more frequently found in malignant pleural effusions (MPE)-associated lung adenocarcinoma than in lung adenocarcinoma or squamous cell carcinoma without MPE (P<0.05), indicating that ApoE is associated with the pathogenesis of MPE in patients with lung adenocarcinoma. Next, we examined the roles of ApoE in an MPE-derived lung adenocarcinoma cell line that endogenously over-expresses ApoE, PC14PE6/AS2 (AS2). In that experiment we inhibited ApoE expression by transfection of a plasmid carrying ApoE siRNAs into AS2 cells to generate AS-S2 and AS-S3 cells. Compared to vector-control cells and parental AS2 cells, AS2-S2 and AS2-S3 cells grew slower (P<0.05), were more sensitive to cisplatin, and had significantly impaired cellular migration (P<0.05). Furthermore, over-expression of ApoE was independently associated with poor survival in lung adenocarcinoma patients who had MPE at the time of diagnosis (P<0.001). Conclusively, ApoE over-expression promotes cancer proliferation and migration and contributes to an aggressive clinical course in patients with lung adenocarcinoma and MPE.
机译:许多人类肺癌细胞系表达载脂蛋白E(ApoE),尤其是肺腺癌患者中源自恶性胸腔积液(MPE)的细胞。这项研究旨在调查ApoE表达对肺癌的影响。在肺癌组织中,与无MPE的肺腺癌或鳞状细胞癌相比,在恶性胸腔积液(MPE)相关的肺腺癌中发现ApoE的频率更高(P <0.05),这表明ApoE与患者MPE的发病机制有关与肺腺癌。接下来,我们检查了ApoE在MPE衍生的内源性过表达ApoE,PC14PE6 / AS2(AS2)的肺腺癌细胞系中的作用。在该实验中,我们通过将携带ApoE siRNA的质粒转染到AS2细胞中以产生AS-S2和AS-S3细胞来抑制ApoE表达。与载体对照细胞和亲本AS2细胞相比,AS2-S2和AS2-S3细胞生长较慢(P <0.05),对顺铂更敏感,并且显着损害细胞迁移(P <0.05)。此外,在诊断时患有MPE的肺腺癌患者中,ApoE的过表达与生存不良相关(P <0.001)。结论是,ApoE的过度表达促进了癌症的扩散和迁移,并促进了肺腺癌和MPE患者的临床进程。

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