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

Author:

Li Shengli1,Guo Wenwen1,Geng Huayun2,Wang Chao3,Yang Shuige1,Xu Xinxin4ORCID

Affiliation:

1. Department of Hematology, Jining No.1 People’s Hospital, No. 6 Health Road, Rencheng District, Jining 272100, Shandong, China

2. Department of Hematology, Dongchangfu People’s Hospital of Liaocheng, 281 Dongguan Street, Dongchangfu District, Liaocheng 252000, Shandong, China

3. Department of Emergency, Zi Bo Central Hospital, 54 Communist Youth League West Road, Zhangdian District, Zibo 255000, Shandong, China

4. Department of Hematology, Zi Bo Central Hospital, 54 Communist Youth League West Road, Zhangdian District, Zibo, 255000 Shandong, China

Abstract

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.

Publisher

Portland Press Ltd.

Subject

Cell Biology,Molecular Biology,Biochemistry,Biophysics

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