Objective To detect the expression characteristics of lncRNA SNHG16 in hepatocellular carcinoma, and observe the proliferation regulatory effect by miR-141-3p/FOXJ3 on the hepatocarcinoma cells. Methods Potential binding sites were predicted between SNHG16 and miR-141-3p, miR-141-3p and FOXJ3 by bioinformatics analyses. Forty-nine cases of hepatocellular carcinoma were collected, the tumor tissue and the adjacent liver tissue were retained. The normal human hepatocyte HL-7702, hepatocarcinoma cells of Hep-3B and Huh7 were selected. The pc-DNA3.1-SNHG16 group, si-SNHG16 group, miR-141-3p inhibitor group, miR-141-3p mimic group, and si-FOXJ3 group were constructed The cell proliferation activity was detected through CCK-8 method. The expression of SNHG16 and miR-141-3p was detected by real-time fluorescence quantitative PCR(qRT-PCR), FOXJ3 and Ki67 were detected through immunohistochemistry method, FOXJ3 were detected by Western blot. Target relationship was verified between SNHG16 and miR-141-3p, miR-141-3p and FOXJ3 by double luciferase reporter gene experiment. Results Possible combination of base sequences were found between SNHG16 and miR-141-3p, miR-141-3p and FOXJ3 by bioinformatics analysis. The expression of SNHG16 and FOXJ3 were higher in human hepatoma cell line than in normal hepatocyte line. The expression of miR-141-3p was lower in human hepatoma cell line than that in normal hepatocyte line. Compared with the control group and the empty vector transfection group, the proliferation activity was increased at 48h in pc-DNA3.1-SNHG16 group, while it was decreased in si-SNHG16 group, which lasted to 96h. Target relationship was found between SNHG16 and miR-141-3p, miR-141-3p and FOXJ3 in double luciferase reporter gene test. The rescue experiment showed that the inhibition of miR-141-3p could partially reverse the inhibition effect of si-SNHG16 and si-FOXJ3 on cell proliferation. The expression of SNGHN16 and the positive rate of FOXJ3 in hepatocellular carcinoma were significantly higher than that in adjacent liver tissues, and the expression of miR-141-3p was significantly lower than that in adjacent liver tissues. SNHG16 was negatively correlated with miR-141-3p, miR-141-3p and FOXJ3, and positively correlated with FOXJ3 and Ki67 in hepatocellular carcinoma. Conclusion Expression of SNHG16 is increased in hepatocellular carcinoma, which promotes the proliferation through miR-141-3p/FOXJ3 pathway.