Department of Hematology, Jining No.1 People's Hospital, No. 6 Health Road, Rencheng District, Jining 272100, Shandong, China.
Department of Hematology, Dongchangfu People's Hospital of Liaocheng, 281 Dongguan Street, Dongchangfu District, Liaocheng 252000, Shandong, China.
Biosci Rep. 2020 May 29;40(5). doi: 10.1042/BSR20193631.
T-cell acute lymphoblastic leukemia (T-ALL) is a malignant disease arising from the abnormal proliferation of T lymphocyte in marrow. Long non-coding RNAs (lncRNAs) are one kind of non-coding RNAs (ncRNAs), which were reported to modulate the initiation or progression of diverse cancers. However, the role of LINC00511 in T-ALL was unknown. To figure out the function and mechanism of LINC00511 in T-ALL, a series of experiments were carried out. Based on the experimental results, we discovered that LINC00511 boosted cell proliferation and invasion, but hindered cell apoptosis in T-ALL cells. Besides, based on bio-informatics tool, miR-195-5p was selected for further exploration. Then, miR-195-5p was validated to bind with LINC00511. Hereafter, LRRK1 was testified to serve as a target gene of miR-195-5p. At last, rescue assays suggested that LRRK1 overexpression restored sh-LINC00511#1-mediated effects on cell proliferation and apoptosis. All in all, LINC00511 exacerbated T-ALL progression via miR-195-5p/LRRK1 axis, implying a potential therapeutic clue for the patients with T-ALL.
T 细胞急性淋巴细胞白血病(T-ALL)是一种起源于骨髓中 T 淋巴细胞异常增殖的恶性疾病。长链非编码 RNA(lncRNA)是一种非编码 RNA(ncRNA),据报道,它可以调节多种癌症的发生或进展。然而,LINC00511 在 T-ALL 中的作用尚不清楚。为了研究 LINC00511 在 T-ALL 中的功能和机制,进行了一系列实验。基于实验结果,我们发现 LINC00511 促进了 T-ALL 细胞的增殖和侵袭,但抑制了细胞凋亡。此外,基于生物信息学工具,选择了 miR-195-5p 进行进一步探索。随后,验证了 miR-195-5p 与 LINC00511 结合。此后,证实 LRRK1 是 miR-195-5p 的靶基因。最后,挽救实验表明,LRRK1 的过表达恢复了 sh-LINC00511#1 对细胞增殖和凋亡的调节作用。总之,LINC00511 通过 miR-195-5p/LRRK1 轴加剧了 T-ALL 的进展,为 T-ALL 患者提供了一种潜在的治疗线索。