Background: LINC00958 is involved in bladder cancer, but its mechanism of action remains indistinct. This study further analyzed its potential targets, aiming to search for therapeutic targets. Materials and Methods: miR-378a-3p was predicted to bind to LINC00958 and IGF1R, which was verified by double-luciferase reporter analysis. The levels of LINC00958 and miR-378a-3p in bladder cancer tissues and cells, and their correlation were further analyzed. Then LINC00958, miR-378a-3p, and IGF1R in bladder cancer cells were up- or downregulated, and their effects on cell viability, migration, and invasion of cells were detected, respectively. Results: LINC00958 binds to miR-378a-3p whose target gene was IGF1R. The expression of miR-378a-3p was negative relative with the level of LINC00958 and IGF1R. Overexpressed miR-378a-3p restrained the activity, migration, and invasion of bladder cancer cells, which was the same as the effects of silent LINC00958 and downregulated IGF1R. Nonetheless, upregulated LINC00958 rescued the antitumor effect of overexpressed miR-378a-3p, whereas miR-378a-3p inhibitor acted as a cancer promoter to reverse the inhibition of downregulated IGF1R on cell activity, migration, and invasion. Conclusion: LINC00958 accelerated the propagation and metastasis of bladder cancer cells through sponging miR-378a-3p to elevate IGF1R, which might trigger a new direction for the treatment of bladder cancer.