Hensen et al. found that targeted disruption of the murine Plag1 could cause growth retardation. In recent microarray analyses, genes were identified that are consistently induced or repressed by PLAG1, and these were classified into various functional categories. Using the KEGG database we searched for pathways where the miR-141 target genes function in order to gain insight into the processes that could be affected by the dysregulated miR-141. The target genes of miR-141 were involved in several important signaling pathways, i.e. MAPK signaling pathway and Wnt signaling pathway. MAPK signaling pathway is implicated in regulating cell growth and differentiation. Decreased MAPK signaling can contribute to defective placental development. Mutation in this signaling cascade lead to defects in the placental labyrinthine region. Additionally, Wnt signaling has been implicated in the regulation of cell proliferation, apoptosis and cell fate. This pathway also played a critical role in both initiating and patterning of the anterior-posterior axis, which precedes gastrulation during mouse embryonic development. Aberrant expression of miR-141 might inactivate these two important pathways, consequently affecting placental development and fetal growth. Further study of MAPK and Wnt pathway may have implications for understanding the pathogenesis of FGR. Downstream effects of miRNA on post-transcriptional gene regulation remain more challenging and require use of bioinformatics approaches to first AbMole 4-(Aminomethyl)benzoic acid predict mRNA targets of specific miRNA and then confirm the effects of over- or under-expression of miRNA on that particular target. Due to the miRNAs’ ultimate role in controlling protein translation, true confirmation of targets requires examination of the proteins of interest using specific antibodies, or through in-vitro approaches coupling targeted miRNA binding regions to reporter constructs. The understanding of miRNAs’role in the human placenta is in its infancy but due to the known critical role of miRNA in human development, it is certainly an attractive and exciting field of study. Our study has several limitations. The most important limitation is the size of the population studied. The sample size of our present study was relatively small. Future studies with larger sample size are needed to validate this association. Secondly, our results were based on unadjusted estimates, while a more precise analysis should be conducted if all individual data were available, which would allow for the adjustment by other co-variants including age, body mass index, smoking status, drinking status, and other lifestyle factors. Thirdly, only one AbMole UNC2881 miRNAs were involved in our study, while more miRNAs should be evaluated in the future, for instance identifying the miRNAs expression profiling using microarray assay. Our data are the first to indicate that miR-141 was significantly upregulated in placental tissues of FGR compared with normal controls. In particular, we have demonstrated that the significantly increased miR-141 could serve as adjunct biomarkers for the diagnosis of FGR. Additionally, we propose the effect of up-regulated miR-141 contribute to FGR may through down regulation of E2F3 expression at post-transcriptional level and PLAG1 expression at both transcriptional and post-transcriptional level. These results provide novel information regarding the molecular mechanism of FGR and the clinical value of miR-141 pertinent to FGR.