The liver is an essential metabolic organ that maintains numerous vital functions in the body. The regulatory mechanisms of hepatogenesis are complex, involving many growth factors and transcription factors across three stages- hepatic specification, differentiation and outgrowth. miRNAs are known to be important genetic regulators in development. Less is known about which miRNAs participate in embryonic hepatic outgrowth. Dysregulation of miR-145 has been shown to promote pathological liver growth. However, the regulatory mechanism of miR-145 in embryonic liver development remains unclear. In this study, we demonstrated a significant decrease in miR-145 expression during hepatogenesis. We modulated miR-145 expression in zebrafish embryos using a miR-145 mimic or a miR-145 hairpin inhibitor. Impaired embryonic liver morphogenesis was observed in response to altered miR-145 expression. We further confirmed a critical role of miR-145 in hepatic outgrowth, but not in liver specification and differentiation, by whole-mount in situ hybridization. Loss of miR-145 expression promoted hepatic cell proliferation, and vice versa. Our previous studies identified a growth factor, Progranulin A (GrnA), which regulates zebrafish hepatic outgrowth through MET signaling. We further revealed that GrnA is a target of miR-145 and MET signaling is also regulated by miR-145, which was verified by luciferase reporter assay and gene expression analysis. In addition, co-injection of GrnA mRNA with miR-145 mimic or MO-grnA with miR-145 inhibitor could restore the liver defects caused by dysregulation of miR-145 expression. In conclusion, our findings identified a functional role of miR-145 in zebrafish hepatic outgrowth through regulating GrnA signaling. This mechanism may be a new therapeutic target for liver failure and liver cancer.