We aimed to systematically evaluate the regulatory effect of arsenic on wnt/β-catenin signaling pathway and to provide theoretical basis for revealing the mechanism of the relationship between arsenic and cell proliferation. The meta-analysis was carried out using Revman5.2 and Stata13.0 to describe the differences between groups with standard mean difference. We found in normal cells that the levels of wnt3a, β-catenin, glycogen synthase kinase-3β phosphorylated at serine 9 (p-GSK-3β(Ser9)), cyclinD1, proto-oncogene c-myc, and vascular endothelial growth factor (VEGF) in the arsenic intervention group were higher than those in the control group, and the level of glycogen synthase kinase-3β (GSK-3β) was lower than that in the control group (P < 0.05, respectively). Subgroup analysis showed that for a long time period (>24 h), the level of β-catenin in the arsenic intervention group was higher than that in the control group, and the level of GSK-3β of the same long-time period (>24 h) with low-dose (≤5 μM) intervention was lower than those in the control group (P < 0.05, respectively). In cancer cells, the levels of β-catenin, cyclinD1, c-myc, and VEGF in the arsenic intervention group were lower than those in the control group, while the level of GSK-3β in the arsenic intervention group was higher than that in the control group (P < 0.05, respectively). Subgroup analysis showed that the levels of β-catenin, cyclinD1, and c-myc in the high-dose (>5 μM) arsenic intervention group were lower than those in the control group, and the levels of β-catenin and cyclinD1 in the high-dose (>5 μM) arsenic intervention group were lower than those in the low-dose (≤5 μM) arsenic intervention group (P < 0.05, respectively). In addition, the regulation of arsenic on β-catenin was dose-dependent in the range of arsenic concentration from 0 to 7.5 μM. This study revealed that arsenic could upregulate wnt/β-catenin signaling pathway in normal cells and downregulate it in cancer cells, and its effect was affected by time and dose.