长链非编码RNA511对骨肉瘤Saos-2细胞增殖、迁移与凋亡的影响和机制

Effects and mechanism of long non-coding RNA511 on proliferation,migration and apoptosis of osteosarcoma Saos-2 cells

目的:探讨长链非编码RNA511(LINC00511)对人骨肉瘤细胞Saos-2增殖、凋亡与迁移的影响及其作用机制。方法:将Saos-2细胞感染LINC00511过表达的慢病毒,获得稳定感染的细胞株。LI NC00511过表达后,进行CCK-8细胞增殖实验、细胞克隆形成实验、细胞凋亡实验、细胞划痕实验等观察LINC00511对Saos-2细胞增殖、凋亡以及迁移的影响。利用蛋白质印迹法检测上皮-间质转化(epithelial-mesenchymal transition,EMT)相关蛋白质E-cadherin、Vimentin和α-SMA的表达,以及PI3K/Akt信号通路中PI3K和p-Akt的蛋白质表达量,探讨LINC00511抑制骨肉瘤细胞增殖、迁移的分子调控机制。结果:Saos-2细胞中过表达LINC00511能够显著抑制骨肉瘤细胞增殖、迁移,促进细胞凋亡。Saos-2细胞中的E-cadherin蛋白表达显著升高,而Vimentin和α-SMA蛋白表达显著降低,骨肉瘤细胞的EMT受到显著抑制。此外,PI3K和p-Akt(308)蛋白表达显著降低,而p-Akt(473)蛋白表达并无明显变化,PI3K/Akt信号通路受到明显抑制。结论:LINC00511通过抑制骨肉瘤细胞的EMT以及PI3K/Akt信号通路对骨肉瘤细胞增殖、迁移产生调控作用。LINC00511可作为骨肉瘤的潜在生物标志物和新的治疗靶点。

Objective:To investigate the effects of long non-coding RNA 511(LINC00511) on proliferation,apoptosis,and migration of human osteosarcoma cell line Saos-2 and its mechanism.Methods:Saos-2 cells were infected with LINC00511 overexpression lentivirus to obtain a stable infected cell line.After overexpression of LINC00511,the effects of LINC00511 on proliferation,apoptosis,and migration of Saos-2 cells were observed by CCK-8 cell proliferation assay,cell clone formation assay,apoptosis assay and cell scratch assay.Western blotting was used to detect the expression of EMT related proteins E-cadherin,Vimentin and α-SMA,as well as the protein expression of PI3 K and p-Akt in PI3 K/Akt signaling pathway,so as to explore the molecular regulatory mechanism of LINC00511 inhibiting the proliferation and migration of osteosarcoma cells.Results:Overexpression of LINC00511 in Saos-2 cells significantly inhibited the proliferation and migration of osteosarcoma cells and promoted cell apoptosis.The expression of E-cadherin protein in Saos-2 cells was significantly increased,while Vimentin and α-SMA protein expression was significantly decreased.EMT of osteosarcoma cells was significantly inhibited.In addition,the expression of PI3 K and p-Akt(308) protein was significantly decreased,while p-Akt(473) protein expression was not significantly changed,and PI3 K/Akt signaling pathway was significantly inhibited.Conclusion:LINC00511 regulates the proliferation and migration of osteosarcoma cells by inhibiting EMT and PI3 K/Akt signaling pathway.LINC00511 can be used as a potential biomarker and a new therapeutic target for osteosarcoma.