Background Long non-coding RNA (lncRNA) plays a pivotal role in bone regeneration by interaction with microRNAs (miRNAs) and constructing a lncRNA-miRNA regulatory network. Objectives This research aimed to elucidate the role of lncRNA CASC11 in the delayed healing process of tibial fractures and to explore its potential regulatory mechanisms. Materials and methods The expression levels of CASC11 and miR-150-3p in serum samples were detected and the predictive capability of CASC11 regarding delayed healing in fracture patients. Furthermore, the study confirmed the accuracy of the binding sites between CASC11 and miR-150-3p. Subsequently, overexpression/interference plasmids of CASC11, along with overexpression plasmids co-transfected with both CASC11 and miR-150-3p, were systematically introduced into MC3T3-E1 cells to investigate their effects on the expression of osteogenic marker genes, as well as their influence on cellular proliferation and apoptosis. Results The expression levels of CASC11 were significantly elevated, while miR-150-3p levels were markedly decreased in individuals exhibiting delayed fracture healing (P < 0.001). CASC11 was observed to suppress the expression of osteogenic marker genes, inhibit the proliferation of MC3T3-E1 cells, and promote cell apoptosis (P < 0.05). Furthermore, the overexpression of miR-150-3p effectively countered the inhibitory impact of CASC11 on osteogenic differentiation and the promoting effect on cell apoptosis (P < 0.05). Conclusion The sponging effect of CASC11 on miR-150-3p led to delayed fracture healing. CASC11 emerges as a potential target for treating delayed fracture healing.