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RASL10A是小GTP酶RAS亚家族的成员之一,可抑制人肺腺癌A549细胞的上皮-间质转化和侵袭。

RASL10A, a member of the RAS subfamily of small GTPases, suppresses the EMT and invasion of human lung adenocarcinoma A549 cells.

作者信息

Nishizuka Makoto, Nakajima Kanae, Odagiri Chie, Wada Nanaka, Sakai Satoshi

机构信息

Department of Applied Biology and Food Sciences, Faculty of Agriculture and Life Science, Hirosaki University, 3 Bunkyo-cho, Hirosaki, Aomori, Japan.

Department of safety of foods and chemicals, Graduate School of Sustainable Community Studies, Hirosaki University, 3 Bunkyo-cho, Hirosaki, Aomori, Japan.

出版信息

Biosci Biotechnol Biochem. 2025 Jun 23;89(7):945-953. doi: 10.1093/bbb/zbaf052.

Abstract

Lung adenocarcinoma (LUAD) is the most frequently diagnosed form of non-small cell lung cancer and is known to develop distant metastases, such as brain and bone metastases, which can considerably affect the prognosis of patients. Therefore, there is a need to elucidate the metastatic mechanisms of LUAD and establish treatments to control metastasis. In this study, Kaplan-Meier plotter analysis demonstrated that patients with LUAD and low RASL10A expression have a poor prognosis. Furthermore, loss or gain of function experiments revealed that RASL10A suppresses transforming growth factor-beta (TGF-β)-induced epithelial-mesenchymal transition (EMT) and the subsequent invasion of LUAD A549 cells. In addition, we found that RASL10A suppresses Smad3 phosphorylation and Snail expression during the early stages of EMT. These results indicate that RASL10A is a novel factor that inhibits TGF-β signaling-mediated EMT and invasion in A549 cells. RASL10A has the potential to become a new therapeutic target for patients with LUAD.

摘要

肺腺癌(LUAD)是最常被诊断出的非小细胞肺癌类型,已知会发生远处转移,如脑转移和骨转移,这会严重影响患者的预后。因此,有必要阐明LUAD的转移机制并建立控制转移的治疗方法。在本研究中,Kaplan-Meier绘图仪分析表明,LUAD患者且RASL10A表达低的患者预后较差。此外,功能丧失或获得实验表明,RASL10A可抑制转化生长因子-β(TGF-β)诱导的上皮-间质转化(EMT)以及随后LUAD A549细胞的侵袭。此外,我们发现RASL10A在EMT早期抑制Smad3磷酸化和Snail表达。这些结果表明,RASL10A是一种新型因子,可抑制TGF-β信号介导的A549细胞EMT和侵袭。RASL10A有潜力成为LUAD患者的新治疗靶点。

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