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. 2021 Mar 18;11:628353. doi: 10.3389/fonc.2021.628353

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Copyright © 2021 Gu, Huang, Zhang, Wang, Tao, Yang, Zheng, Liu, Yang, Zhu, Wang and Fan.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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TMPRSS4 activated the ERK1/2 signaling pathway in pancreatic cancer. (A) GSEA indicates a significant association between the mRNA expression levels of TMPRSS4 and the MAPKs pathways, in particular, the ERK1/2 signaling pathway in pancreatic cancer. The other two classical signal pathways of MAPKs, that is, JNK and p38, showed no positive correlation with TMPRSS4. (B) Western blot analysis of TMPRSS4, total ERK1/2, phosphorylated ERK1/2, Bax, Bcl-2, and cleaved caspase 3; in the indicated cells. β-actin was used as a loading control. Each bar represents the mean ± SD of three independent experiments. Paired Student's t-test was applied. ^*P < 0.05; ^**P < 0.01; ^***P < 0.001; GSEA, Gene Set Enrichment Analysis; MAPKs, Mitogen-activated Protein Kinases.