LINC00284通过miR-3127/STAT3轴促进急性T淋巴细胞白血病细胞增殖、迁移和侵袭

LINC00284 promotes the proliferation,migration and invasion of acute T-lymphoblastic leukemia cells through the miR-3127/STAT3 axis

目的:探讨LINC00284在急性T淋巴细胞白血病(T-cell acute lymphoblastic leukemia,T-ALL)进展中的调节作用和潜在机制。方法:通过RT-qPCR检测T-ALL细胞系中LINC00284、miR-3127和STAT3的表达。将干预LINC00284、miR-3127或STAT3表达的质粒载体转染至MOLT-4细胞,通过MTT和流式细胞术测定细胞增殖和凋亡,通过Transwell测定细胞迁移和侵袭。通过生物信息网站分析和双荧光素酶报告基因检测验证miR-3127和LINC00284或STAT3之间的靶向关系。结果:T-ALL细胞系中LINC00284和STAT3表达上调,miR-3127表达下调。下调LINC00284或上调miR-3127显著抑制T-ALL细胞的增殖、迁移、侵袭,促进细胞凋亡。LINC00284充当miR-3127的分子海绵抑制其表达,miR-3127靶向负调控STAT3表达。上调STAT3可以逆转下调LINC00284对T-ALL细胞增殖、迁移、侵袭的抑制作用和对细胞凋亡的促进作用。结论:这些发现表明LINC00284通过调控miR-3127/STAT3轴促进T-ALL细胞增殖、迁移、侵袭,抑制细胞凋亡,这可能为T-ALL治疗提供新的靶点。

Objective:To explore the regulatory role and potential mechanism of LINC00284 in the progression of T-cell acute lymphoblastic leukemia(T-ALL).Methods:The expression of LINC00284,miR-3127 and STAT3 in T-ALL cell lines were detected by RT-qPCR.Plasmid vectors that interfere with the expression of LINC00284,miR-3127 or STAT3 were transfected into MOLT-4 cells.Cell proliferation and apoptosis were measured by MTT and flow cytometry,and cell migration and invasion were measured by Transwell.The targeting relationship between miR-3127 and LINC00284 or STAT3 was verified through bioinformatics website analysis and dual luciferase reporter gene testing.Results:In T-ALL cell lines,the expression of LINC00284 and STAT3 were upregulated,while the expression of miR-3127 was downregulated.Downregulation of LINC00284 or upregulation of miR-3127 significantly inhibits the proliferation,migration,and invasion of T-ALL cells,promoting cell apoptosis.LINC00284 acts as a molecular sponge for miR-3127,which targets and negatively regulates STAT3 expression.Upregulation of STAT3 can reverse the inhibitory effect of downregulation of LINC00284 on the proliferation,migration,invasion,and promotion of apoptosis of T-ALL cells.Conclusion:These findings suggest that LINC00284 promotes the proliferation,migration,invasion,and inhibition of apoptosis of T-ALL cells by regulating the miR-3127/STAT3 axis,which may provide a new target for T-ALL treatment.