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. 2017 Jun 27;8(37):61742–61760. doi: 10.18632/oncotarget.18687

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Copyright: © 2017 Han et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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(A) Western blot analysis showed that the protein level of P-ERK in the STMN1 group was significantly higher than that of the control group. (B) RT-PCR analysis of the mRNA levels of ERK downstream transcription factors such as FOS, EGR1, and JUN revealed significantly higher levels in the STMN1group than in the control group. (C) KYSE 170-STMN1 cells were treated with ERK inhibitors AZD8330; western blot analysis showed that ERK phosphorylation was inhibited. (D) The effects of ERK phosphorylation on the migration ability of KYSE 170-STMN1 cells were analyzed by wound-healing assay. The results showed that inhibition of ERK phosphorylation in KYSE 170-STMN1 cells markedly reduced cell motility. (E) Stathmin expression in KYSE 510 and (F) KYSE 170-STMN1 cells was knocked down by two different STMN1-specific siRNAs (siRNA-1 and siRNA-2), and the activation of the integrinα5β1/FAK/ERK pathway was measured by immunoblotting (ns, P>0.05; *, P<0.05; ***, P<0.001).