Objective To explore the effect of miR⁃335⁃3p for targeted regulating early growth response factor 1 (EGR1) in the pathogenesis of recurrent abortion (RA). Methods RA⁃related differentially expressed miRNA and regulating⁃EGR1 miRNA were screened through bioinformatics analysis; in addition, the intersection of both was obtained, and binding sites between targeted miRNA and EGR1 were predicted. Targeted effects of miR⁃335⁃3p on EGR1 were validated by using dual luciferase reporter gene assay. The miR⁃335⁃3p inhibitor and inhibitor NC were transfected into human trophoblast cells HTR⁃8/SVneo (setting as the miR⁃335⁃3p inhibitor group and the inhibitor NC group, respectively), and the knockdown efficiency of miR⁃335⁃3p was detected by real⁃time fluorescent quantitative PCR. CCK⁃8 test, cell scratch test, Transwell test and flow cytometry were adopted to detect the proliferation activity, migration ability, invasion ability and apoptosis of cells from the miR⁃335⁃3p inhibitor group and the inhibitor NC group, respectively. Results There were 3 binding sites between miR⁃335⁃3p and EGR1. Dual luciferase reporter gene assay confirmed that miR⁃335⁃3p negatively regulated targeted gene EGR1. The results of real⁃time fluorescent quantitative PCR revealed that the expression of miR⁃335⁃3p in the miR⁃335⁃3p inhibitor group was lower than that in the inhibitor NC group (P<0.05). Cell experiments results indicated that the relative survival rate, migration rate and migration number of cells in the miR⁃335⁃3p inhibitor group were lower or less than those in the inhibitor NC group, while the late apoptosis rate and overall apoptosis rate were higher than those in the inhibitor NC group (P<0.05). Conclusion MiR⁃335⁃3p negatively regulates the expression of EGR1 and affects the function of trophoblast cells. Knockdown of miR⁃335⁃3p expression can inhibit the proliferation, migration or invasion of trophoblast cells and promote cell apoptosis, which may be an important mechanism of miR⁃335⁃3p involved in the occurrence of RA.

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