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

被引:11
|
作者
Li, Shengli [1 ]
Guo, Wenwen [1 ]
Geng, Huayun [2 ]
Wang, Chao [3 ]
Yang, Shuige [1 ]
Xu, Xinxin [4 ]
机构
[1] Jining 1 Peoples Hosp, Dept Hematol, 6 Hlth Rd, Jining 272100, Shandong, Peoples R China
[2] Dongchangfu Peoples Hosp Liaocheng, Dept Hematol, 281 Dongguan St, Liaocheng 252000, Shandong, Peoples R China
[3] Zi Bo Cent Hosp, Dept Emergency, 54 Communist Youth League West Rd, Zibo 255000, Shandong, Peoples R China
[4] Zi Bo Cent Hosp, Dept Hematol, 54 Communist Youth League West Rd, Zibo 255000, Shandong, Peoples R China
关键词
LONG NONCODING RNA; CANCER; CHONDROCYTE; MECHANISMS;
D O I
10.1042/BSR20193631
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
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页数:11
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