OBJECTIVE: Cervical cancer (CC) is a common type of fatal gynecological cancer worldwide. The aim of this study was to identify the exact role of IncRNA CASC15 in the progression of CC and to explore the possible underlying mechanism. PATIENTS AND METHODS: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was used to detect CASC15 expression in 4 CC cell lines, and 54 paired CC tissue samples. The roles of CASC15 in CC were explored through apoptosis assay, colony,formation assay, and proliferation assay in vitro, respectively. Furthermore, the underlying mechanism of CASC15 in CC was explored by luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay. RESULTS: CASC15 expression in CC tissues was remarkably higher than that of adjacent normal tissues. The knockdown of CASC15 significantly inhibited CC cell proliferation, whereas induced cell apoptosis in vitro. Meanwhile. CC cell proliferation was remarkably promoted, and cell apoptosis was inhibited by overexpression of CASC15 in vitro. In addition, miR-101-3p was up-regulated and down-regulated after knockdown and overexpression of CASC15 in vitro, respectively. Furthermore, bioinformatics analysis and mechanism assays revealed that miR-101-3p was a direct target of CASC15 in CC tumorigenesis. CONCLUSIONS: CASC15 could promote proliferation and inhibit apoptosis of CC cells by targeting miR-101-3p. Our findings suggested that CASC15 might offer a new therapeutic intervention for CC patients.