Neuron specific enolase promotes tumor metastasis by activating the Wnt/β-catenin pathway in small cell lung cancer.
Neuron specific enolase promotes tumor metastasis by activating the Wnt/β-catenin pathway in small cell lung cancer.
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神经元特异性烯醇化酶通过激活小细胞肺癌中的 Wnt/β-catenin 通路促进肿瘤转移
DOI:
10.1016/j.tranon.2021.101039
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发表时间:
2021-04
影响因子:
5
通讯作者:
Liu G
中科院分区:
文献类型:
--
作者:
Zha Z;Li D;Zhang P;Wang P;Fang X;Liu X;Weng C;Li B;Wu Y;Mao H;Wang L;Xu L;Dong J;Guan M;Lu L;Liu G
NSE expression was positively correlated with distant metastasis of SCLC. NSE promotes migration, invasion and EMT process of SCLC cells. Wnt/β-catenin signaling pathway is activated in the NSE-overexpressing SCLC cells. NSE interacts with β-catenin and inhibits the degradation of β-catenin. Neuron-specific enolase (NSE) has been used as a specific biomarker for small cell lung cancer (SCLC) patients. Nevertheless, the biological function and mechanism of NSE in SCLC are still unclear. In this study, we clarified the role of NSE in the progression of SCLC and found that NSE expression was positively correlated with distant metastasis. Functional analysis showed that overexpression of NSE promoted migration and invasion of SCLC cells. Mechanism analysis showed that NSE overexpression induced epithelial-mesenchymal transition (EMT) of SCLC cells. Moreover, overexpression of NSE increased the protein expression of β-catenin and its downstream target genes, and silencing β-catenin eliminated NSE-mediated cell migration, invasion and EMT process. Furthermore, NSE interacted with β-catenin and inhibited the degradation of β-catenin. Besides, the animal experiments also indicated that NSE could promote the EMT process and distant metastasis of SCLC cells in vivo. In summary, our results revealed that NSE could promote the EMT process of SCLC cells by activating the Wnt/β-catenin signaling pathway, thereby promoting cell migration, invasion and distant metastasis, which might serve as a potential target for the therapy of SCLC patients.
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影响因子:
15.9
作者:
Chockley, Peter J.;Chen, Jun;Keshamouni, Venkateshwar G.
通讯作者:
Keshamouni, Venkateshwar G.
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:
Pujol, JL;Boher, JM;Quantin, X
通讯作者:
Quantin, X
DOI:
10.1016/j.jtho.2016.01.012
发表时间:
2016-04
期刊:
Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
影响因子:
--
作者:
Bunn PA Jr;Minna JD;Augustyn A;Gazdar AF;Ouadah Y;Krasnow MA;Berns A;Brambilla E;Rekhtman N;Massion PP;Niederst M;Peifer M;Yokota J;Govindan R;Poirier JT;Byers LA;Wynes MW;McFadden DG;MacPherson D;Hann CL;Farago AF;Dive C;Teicher BA;Peacock CD;Johnson JE;Cobb MH;Wendel HG;Spigel D;Sage J;Yang P;Pietanza MC;Krug LM;Heymach J;Ujhazy P;Zhou C;Goto K;Dowlati A;Christensen CL;Park K;Einhorn LH;Edelman MJ;Giaccone G;Gerber DE;Salgia R;Owonikoko T;Malik S;Karachaliou N;Gandara DR;Slotman BJ;Blackhall F;Goss G;Thomas R;Rudin CM;Hirsch FR
通讯作者:
Hirsch FR
影响因子:
2.9
作者:
Bae, Woo-Jin;Lee, Sang-Hyuk;Lim, Young-Chang
通讯作者:
Lim, Young-Chang