Cx31.1 acts as a tumour suppressor in non-small cell lung cancer (NSCLC) cell lines through inhibition of cell proliferation and metastasis.
Cx31.1 acts as a tumour suppressor in non-small cell lung cancer (NSCLC) cell lines through inhibition of cell proliferation and metastasis.
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Cx31.1 通过抑制细胞增殖和转移在非小细胞肺癌 (NSCLC) 细胞系中充当肿瘤抑制剂
DOI：
10.1111/j.1582-4934.2011.01389.x
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发表时间：
2012-05
影响因子：
5.3
通讯作者：
Huang Y
中科院分区：
文献类型：
--
作者：
Zhang D;Chen C;Li Y;Fu X;Xie Y;Li Y;Huang Y
连接蛋白表达减少和间隙连接功能丧失是许多癌症（包括肺癌）的特征。然而，关于Cx31.1与肺癌的关系的报道很少。本研究旨在研究Cx31.1对非小细胞肺癌（NSCLC）的影响。我们发现Cx31.1在NSCLC细胞系中表达下调，并且表达水平与其转移潜能呈负相关。我们在H1299 NSCLC细胞系中异位表达Cx31.1以检测Cx31.1过表达的影响。结果表明，Cx31.1在H1299细胞中的过表达降低细胞增殖，诱导G1期延迟，抑制锚定非依赖性生长，并抑制细胞迁移和侵袭。针对Cx31.1 mRNA的siRNA可部分逆转Cx31.1的细胞周期延迟、细胞迁移和侵袭抑制作用。此外，Cx31.1过表达H1299细胞的异种移植物显示出降低的致瘤性。这些结果表明Cx31.1具有肿瘤抑制特性。进一步的研究表明，cyclin D3可能与Cx31.1诱导的G1期延迟有关。重要的是，Cx31.1增加了上皮标记物（如细胞角蛋白18）的表达，并减少了间充质标记物（如波形蛋白）的表达，表明Cx31.1介导的从间充质向上皮表型的部分转变。结论：Cx31.1抑制NSCLC细胞系的恶性特性，其机制可能包括调控EMT。
Reduced connexin expression and loss of gap junction function is a characteristic of many cancers, including lung cancer. However, there are little reports about the relation between Cx31.1 and lung cancer. This study was conducted to investigate the effect of Cx31.1 on non‐small cell lung cancer (NSCLC). We found that the Cx31.1 was down‐regulated in NSCLC cell lines, and the expression levels were reversely related with their metastatic potential. We ectopically expressed Cx31.1 in H1299 NSCLC cell line to examine the influence of Cx31.1 overexpression. The results showed that overexpression of Cx31.1 in H1299 cells reduced cell proliferation, induced a delay in the G1 phase, inhibited anchorage‐independent growth and suppressed cell migration and invasion. The cell cycle delay and cell migration and invasion suppressive effects of Cx31.1 were partially reversed by siRNA targeting mRNA of Cx31.1. Moreover, xenografts of Cx31.1 overexpressing H1299 cells showed reduced tumourigenicity. These results suggested that Cx31.1 has tumour‐suppressive properties. Further investigation indicated that cyclin D3 may be responsible for Cx31.1‐induced G1 phase delay. Importantly, Cx31.1 increased the expression of epithelial markers, such as cytokeratin 18, and decreased expression of mesenchymal markers, such as vimentin, indicating a Cx31.1‐mediated partial shift from a mesenchymal towards an epithelial phenotype. We concluded that Cx31.1 inhibit the malignant properties of NSCLC cell lines, the mechanisms under this may include regulation of EMT.
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影响因子：
21.3
作者：
Batlle, E;Sancho, E;de Herreros, AG
通讯作者：
de Herreros, AG
影响因子：
5.3
作者：
Cina, Cima;Maass, Karen;Naus, Christian C.
通讯作者：
Naus, Christian C.
DOI：
10.1083/jcb.200601018
发表时间：
2006-03-27
期刊：
The Journal of cell biology
影响因子：
--
作者：
Lee JM;Dedhar S;Kalluri R;Thompson EW
通讯作者：
Thompson EW
影响因子：
64.8
作者：
Elias, Laura A. B.;Wang, Doris D.;Kriegstein, Arnold R.
通讯作者：
Kriegstein, Arnold R.
影响因子：
8
作者：
Al Moustafa, AE;Alaoui-Jamali, MA;Foulkes, WD
通讯作者：
Foulkes, WD