Knockdown of Linc00052 influences osteoblast proliferation,migration and apoptosis

Qi Lu; Wang Junjie; Deng Qingao; Wang Xing

doi:10.12307/2026.655

Abstract：BACKGROUND:Linc00052 is associated with the occurrence and development of various diseases,including cancer and inflammatory diseases.It was found that Linc00052 targets miR-145 to exert a protective effect against human articular chondrocyte injury. OBJECTIVE:To observe the roles of Linc00052 knockdown in the proliferation,migration and apoptosis of osteoblasts. METHODS:(1)Human periapical bone tissues were collected from 30 patients with periapical inflammation and 30 healthy controls.Expression of Linc00052 and miR-145 was detected by RT-qPCR.(2)Passage 3 CP-H111 osteoblasts were cultured in two groups:the experimental group was transfected with lentivirus to knock down the expression of Linc00052,and the control group was transfected with an empty lentiviral negative control.At 72 hours after the transfection,RT-qPCR was used to detect the expression of Linc00052 and miR-145;western blot was used to detect the protein expression of tumor necrosis factor α and transforming growth factor β/SMAD2/SMAD3 signaling pathway proteins;cell counting kit-8 assay was used to detect cell proliferation;cell scratch assay and Transwell assay were conducted to detect cell migration;and flow cytometry was used to detect cell apoptosis. RESULTS AND CONCLUSION:(1)The expression of Linc00052 in periapical bone tissue of periapical periodontitis was significantly higher than that in normal periapical bone tissue(P<0.05).(2)The expression of Linc00052,apoptosis level and protein expression of tumor necrosis factor α in the experimental group were lower than those of the control group(P<0.05),while the protein expression of miR-145,transforming growth factor β1,p-SMAD2,and p-SMAD3 was higher than that in the control group,and the cell migration ability was stronger than that of the control group.To conclude,knockdown of Linc00052 expression can promote osteoblast proliferation and migration and inhibit cell apoptosis by reducing the protein expression of tumor necrosis factor α and activating the transforming growth factor β/SMAD2/SMAD3 signaling pathway.