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. 2022 May 9;14(9):2338. doi: 10.3390/cancers14092338

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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The MBOP/MEK1/pERK/MMP2/MMP9 axis in CRC. (A) MBOP substantially promoted the pERK1/2 in HCT116 and HCT15, but the total ERK expression did not show significant differences. (B) Overexpressing MBOP in HCT116 and HCT15 paved the axis of MBOP/MEK1/pERK/MMP2/MMP9. (C) The signaling pathway axis in animal assay met the expression tendency of in vitro assays (n = 4). (D) HCT116 and HCT15 were treated with the MEK1/2 inhibitor U0126-EtOH for 48 h, and the protein expression of MEK1/2, pERK1/2, and downstream MMP2 and MMP9 all decreased violently. (E) HCT116 cells were transfected with plasmids pcDNA3.1+, pORF-FLAG, and pORFmut-FLAG, followed by treatments of DMSO and U0126-EtOH. The overexpression of MEK1 and MBOP brought by transfecting cells with pORF-FLAG could be partially inhibited by U0126-EtOH, whereas the MAP2K1 showed no significant alterations. Data are presented as mean ± SD, **** p < 0.0001. ns: not significant. (F) The pro-migration effect driven by the transfection of pORF-FLAG could be partially reversed by U0126-EtOH.