Long Noncoding RNA CASC2 Facilitated Wound Healing through miRNA-155/HIF-1α in Diabetic Foot Ulcers

Diabetic foot ulcers (DFU) are among the serious complications which are closely linked to diabetes mellitus. However, there is still a lack of accurate and effective standard prevention and treatment programs for DFU. In this manuscript, we have investigated the function of lncRNA cancer susceptibility candidate 2 (CASC2)/miR-155/hypoxia-inducible factor 1-alpha (HIF-1 alpha) in the wound healing of DFU. We have analyzed lncRNA CASC2`s expression in the marginal tissues of ulcers in patients and mice with DFU. Additionally, the interaction relationship and mechanism between lncRNA CASC2, miR-155, and HIF-1 alpha were determined, which proved the effects of lncRNA CASC2/miR-155/HIF-1 alpha on fibroblasts apoptosis, proliferation, and migration. According to our study, the lncRNA CASC2's expression was low in the tissues of ulcers of DFU mice and patients. lncRNA CASC2's overexpression promoted fibroblasts migration, proliferation, and inhibited apoptosis and was beneficial for the healing of wounds, preferably in the DFU mice. In addition, lncRNA CASC2 directly targets miR-155 and HIF-1 alpha functions as miR-155's target gene. Overexpression of miR-155 abrogated the function of lncRNA CASC2. Similarly, HIF-1 alpha's inhibition has reversed the effect of miR-155 downregulation on fibroblasts. In general, overexpression of lncRNA CASC2 facilitated wound healing through miR-155/HIF-1 alpha in DFU.

Automated summary

In this study, the role of lncRNA CASC2/miR-155/HIF-1 alpha in the wound healing of diabetic foot ulcers (DFU) was investigated. The overexpression of lncRNA CASC2 promoted fibroblasts migration and proliferation, and inhibited apoptosis, benefiting the healing of DFU wounds. Additionally, lncRNA CASC2 directly targeted miR-155 and miR-155's function was associated with HIF-1 alpha.