Orthopedics, Affiliated Hospital of Hebei University, Baoding, 071000, China.
Operating Room, North China University of Science and Technology Affiliated Hospital, Tangshan, 063000, China.
J Orthop Surg Res. 2024 Nov 14;19(1):757. doi: 10.1186/s13018-024-05226-5.
Long non-coding RNA (lncRNA) plays a pivotal role in bone regeneration by interaction with microRNAs (miRNAs) and constructing a lncRNA-miRNA regulatory network.
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.
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.
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).
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.
长链非编码 RNA(lncRNA)通过与 microRNAs(miRNAs)相互作用并构建 lncRNA-miRNA 调控网络,在骨再生中发挥关键作用。
本研究旨在阐明 lncRNA CASC11 在胫骨骨折延迟愈合过程中的作用,并探讨其潜在的调控机制。
检测血清样本中 CASC11 和 miR-150-3p 的表达水平,并预测 CASC11 对骨折患者延迟愈合的能力。此外,研究证实了 CASC11 与 miR-150-3p 结合位点的准确性。随后,系统地将 CASC11 的过表达/干扰质粒以及与 miR-150-3p 共转染的过表达质粒引入 MC3T3-E1 细胞,以研究它们对成骨标记基因表达的影响,以及对细胞增殖和凋亡的影响。
延迟愈合骨折患者的 CASC11 表达水平显著升高,而 miR-150-3p 水平明显降低(P<0.001)。CASC11 被观察到抑制成骨标记基因的表达,抑制 MC3T3-E1 细胞的增殖,并促进细胞凋亡(P<0.05)。此外,miR-150-3p 的过表达有效抵消了 CASC11 对成骨分化的抑制作用和对细胞凋亡的促进作用(P<0.05)。
CASC11 对 miR-150-3p 的海绵作用导致骨折延迟愈合。CASC11 可能成为治疗骨折延迟愈合的潜在靶点。