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. 2019 Oct 22;10(58):6285. doi: 10.18632/oncotarget.27282

Correction: Protein 4.1N acts as a potential tumor suppressor linking PP1 to JNK-c-Jun pathway regulation in NSCLC

Zi Wang 1,2,#, Bianyin Ma 1,#, Hui Li 1,#, Xiaojuan Xiao 1,#, Weihua Zhou 1,3, Feng Liu 2, Bin Zhang 4, Min Zhu 1, Qin Yang 1, Yayue Zeng 1, Yang Sun 5, Shuming Sun 1, Yanpeng Wang 1, Yibin Zhang 1, Haibo Weng 6, Lixiang Chen 6, Mao Ye 5,, Xiuli An 6,7,, Jing Liu 1,
PMCID: PMC6817441  PMID: 31692885

This article has been corrected: During the assembly of Figure 2B, the same image was inadvertently used for both H1299 (pEGFP-C3) and H1299 (pEGFP-4.1N) groups at 0h time point. The proper Figure 2 B specific for H1299 (pEGFP-C3) and H1299 (pEGFP-4.1N) groups are shown below. The authors declare that these corrections do not change the results or conclusions of this paper.

Figure 2. Anti-tumor effects of 4.1N on the proliferation, migration and adhesion in H1299 and 95C cells in vitro.

Figure 2

Both 95C /H1299 cells were transiently transfected with the same amount of human-4.1N shRNA/ pEGFP-4.1N or with the negative control mouse-4.1N shRNA/ null pEGFP vector. (B) More than 90% of the confluent monolayer of transfected cells was scratched and imaged by light microscopy at three time points 0, 12, and 24 h. The degree of motility was shown as percent of wound closure as compare with the 0h time point. The results are the mean ± SD from three independent experiments. Representative images were shown. *indicates p < 0.05 versus control based on the Student’s t-test.

Original article: Oncotarget. 2016; 7:509–523. 509-523. https://doi.org/10.18632/oncotarget.6312


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