Objective To investigate the expression, function and potential mechanism of circular RNA circVCAN(also known as hsa-circ-0073239)in fetal growth restriction (FGR) placenta. Methods The placenta tissue samples were collected from 24 pregnant women (12 with FGR and 12 normal pregnancy) admitted in our hospital from January to December 2018. Real-time quantitative PCR (RT-qPCR) was performed to detect the expression of circVCAN in these placenta samples. Human placental trophoblast cell line HTR8/SVneo was cultured and then transfected with circVCAN interference and overexpression plasmid, respectively. EdU assay, flow cytometer and Transwell assay were carried out respectively to verify the variations in the proliferation, apoptosis and invasion abilities of the cells. And the expression of autophagy related proteins LC3Ⅱ/LC3Ⅰ, ATG5 and ATG7 was measured by Western blotting. Results The expression levels of circVCAN, ATG5, ATG7 and LC3Ⅱ/LC3Ⅰwere significantly higher in FGR placenta tissue than in the normal group (P < 0.01). The termination of pregnancy was earlier in FGR patients than in normal group (P < 0.05), with newborns from the FGR group having lower birth body weight (P < 0.01) and placenta weight (P < 0.05) as well as shorter birth body length (P < 0.01) when compared with those from the normal group. Silencing of circVCAN resulted in enhanced proliferation and invasion abilities in HTR8/SVneo cells (P < 0.01), while circVCAN overexpression led to decreased proliferation and invasion abilities in the cells (P < 0.01), but no statistical difference was seen in the apoptotic rate (P>0.05). The expression levels of autophagy related proteins LC3Ⅱ/LC3Ⅰ, ATG5 and ATG7 were significantly lower in circVCAN interfered cells (P < 0.05), while higher in circVCAN overexpressed cells (P < 0.05). Conclusion CircVCAN is highly expressed in FGR placenta tissue, though it showing no effect on apoptosis but inhibiting the proliferation and invasion of HTR8/SVneo trophoblast cells, and may enhance autophagy by promoting the expression of ATG5 and ATG7.
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