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首页> 外文期刊>Technology in cancer research & treatment. >Overexpression of TRIM25 in Lung Cancer Regulates Tumor Cell Progression
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Overexpression of TRIM25 in Lung Cancer Regulates Tumor Cell Progression

机译:TRIM25在肺癌中的过表达调节肿瘤细胞的进程。

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摘要

Lung cancer is one of the most common causes of cancer-related deaths worldwide. Although great efforts and progressions have been made in the study of the lung cancer in the recent decades, the mechanism of lung cancer formation remains elusive. To establish effective therapeutic methods, new targets implied in lung cancer processes have to be identified. Tripartite motif-containing 25 has been associated with ovarian and breast cancer and is thought to positively promote cell growth by targeting the cell cycle. However, whether tripartite motif-containing 25 has a function in lung cancer development remains unknown. In this study, we found that tripartite motif-containing 25 was overexpressed in human lung cancer tissues. Expression of tripartite motif-containing 25 in lung cancer cells is important for cell proliferation and migration. Knockdown of tripartite motif-containing 25 markedly reduced proliferation of lung cancer cells both in vitro and in vivo and reduced migration of lung cancer cells in vitro. Meanwhile, tripartite motif-containing 25 silencing also increased the sensitivity of doxorubicin and significantly increased death and apoptosis of lung cancer cells by doxorubicin were achieved with knockdown of tripartite motif-containing 25. We also observed that tripartite motif-containing 25 formed a complex with p53 and mouse double minute 2 homolog (MDM2) in both human lung cancer tissues and in lung cancer cells and tripartite motif-containing 25 silencing increased the expression of p53. These results provide evidence that tripartite motif-containing 25 contributes to the pathogenesis of lung cancer probably by promoting proliferation and migration of lung cancer cells. Therefore, targeting tripartite motif-containing 25 may provide a potential therapeutic intervention for lung cancer.
机译:肺癌是全世界与癌症相关的死亡的最常见原因之一。尽管在最近几十年中在肺癌的研究中已经做出了巨大的努力和进展,但是肺癌形成的机制仍然难以捉摸。为了建立有效的治疗方法,必须确定肺癌过程中隐含的新靶标。含有三方基序的25已与卵巢癌和乳腺癌相关,并被认为可通过靶向细胞周期来积极促进细胞生长。但是,含三方基序的25在肺癌的发展中是否具有功能尚不清楚。在这项研究中,我们发现含有三方基序的25在人类肺癌组织中过表达。含三方基序的25在肺癌细胞中的表达对于细胞增殖和迁移很重要。击倒含有三方基序的25在体外和体内均显着降低了肺癌细胞的增殖,并在体外降低了肺癌细胞的迁移。同时,含三重基序的沉默也使阿霉素25的沉默增加,并显着增加了阿霉素对肺癌细胞的死亡和凋亡。在人肺癌组织和肺癌细胞中,p53和小鼠double minutes 2同源物(MDM2)均含有25个沉默,而包含三方基序的沉默增加了p53的表达。这些结果提供了证据,即含有三方基序的25可能通过促进肺癌细胞的增殖和迁移而促进了肺癌的发病。因此,靶向含三方基序的25可能为肺癌提供潜在的治疗干预。

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