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

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, th...

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Bibliographic Details
Published in:Bioscience reports 2020-05, Vol.40 (5)
Main Authors: Li, Shengli, Guo, Wenwen, Geng, Huayun, Wang, Chao, Yang, Shuige, Xu, Xinxin
Format: Article
Language:English
Subjects:
Apoptosis
Biotechnology
Cardiovascular System & Vascular Biology
Cell Line, Tumor
Cell Movement
Cell Proliferation
Gene Expression & Regulation
Gene Expression Regulation, Leukemic
Genomics
Humans
MicroRNAs - genetics
MicroRNAs - metabolism
Neoplasm Invasiveness
Pharmacology & Toxicology
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - enzymology
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - genetics
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - pathology
Protein-Serine-Threonine Kinases - genetics
Protein-Serine-Threonine Kinases - metabolism
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
Signal Transduction
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Summary: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.
ISSN:0144-8463
1573-4935
DOI:10.1042/BSR20193631