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LINC00511 通过 miR-195-5p/LRRK1 轴加剧 T 细胞急性淋巴细胞白血病。

LINC00511 exacerbated T-cell acute lymphoblastic leukemia via miR-195-5p/LRRK1 axis.

机构信息

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.

出版信息

Biosci Rep. 2020 May 29;40(5). doi: 10.1042/BSR20193631.

Abstract

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.

摘要

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。

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