Background It was demonstrated that aberrant expression of long noncoding RNAs (LncRNAs) exerts regulatory effects on several malignancies. The lncRNA CASC7 effect on bladder cancer (BC) was not demonstrated. CASC7 role in BC was investigated in the current study. Material and Methods CASC7 expression was investigated. Using a luciferase reporter test, the link between CASC7, miR-103a-5p, and TFPI2 was confirmed. CCK-8 and flow cytometry assay were utilized for detecting apoptosis and cell viability. Transwell and wound healing tests were utilized for evaluating the invasion and migration cell capabilities. For analyzing the TFPI2, p-GSK-3β, β-catenin, and GSK-3β protein level, western blot was utilized. Results CASC7 expression greatly decreased in BC cell lines and clinical specimens. In function loss and gain assays, CASC7 prevents migration, proliferation, and invasion of the cell and induces cell death in BC cells, in accordance with research. In addition, CASC7 has been reported to enhance TFPI2 expression and negatively regulate the miR-103a-5p expression. Consequently, TFPI2 as a downstream target of miR-103a-5p and miR-103a-5p as a direct target of CASC7 were investigated. Moreover, over-expression of CASC7 markedly reduced the p-GSK-3β, β-catenin, expression. In contrast, the knockdown of CASC7 had the opposite effect. Conclusion Our findings showed that BC CASC7 functions as a tumor suppressor via miR-103a-5p and TFPI2. Its regulatory impact is related to the miR-103a-5p/TFPI2/Wnt/ β-catenin signaling pathway. In the BC treatment, CASC7 can serve as a biomarker or therapeutic target.