The mRNA levels of ERK5 and MAP3K7 were increased in BC tissues compared with noncancerous tissues or NC breast tissues (P<0.
Effect of ectopic miR-143 level on the expression and phosphorylation of ERK5 and MAP3K7 in MCF-7 cells
01), and the mRNA levels of ERK5 and MAP3K7 in cells with miR-143 mimic were remarkably decreased compared with cells with mimic control (P<0.
Effect of ectopic miR-143, ERK5 and MAP3K7 levels on cell growth in MCF-7 cells
In the present study, the level of miR-143 was reduced, while the expression and phosphorylation of ERK5 and MAP3K7 were increased in BC tissues compared with noncancerous tissues or NC breast tissues.
ERK5 is a member of the MAPK family, which has been reported as an enhancer of cell proliferation and progression by mediating the cell cycle, as well as a tumorigenesis (26).
Moreover, we also revealed that miR-143 regulated cyclin D1 expression through down-regulation of ERK5.
In conclusion, the present study reveals that both ERK5 and MAP3K7 may be the target genes of miR-143.
Regulation of cellular functions by the ERK5 signalling pathway.
miR-143 Interferes with ERK5 signaling, and abrogates prostate cancer progression in mice.
ERK5 knockdown generates mouse leukemia cells with low MHC class I levels that activate NK cells and block tumorigenesis.
miR-143 suppresses epithelial-mesenchymal transition and inhibits tumor growth of breast cancer through down-regulation of ERK5.