Effect of LINC00641 on Viability and Apoptosis of Acute Myeloid Leukemia Cells.
10.19746/j.cnki.issn.1009-2137.2025.04.010
- Author:
Yun-Ling ZHANG
1
;
Ying YANG
1
;
Yin SUN
2
;
Hong-Li CHAI
2
Author Information
1. Department of Neonatology,Tengzhou Central People's Hospital, Tengzhou 277500, Shandong Province, China.
2. Department of Pediatrics, Tengzhou Central People's Hospital, Tengzhou 277500, Shandong Province, China.
- Publication Type:Journal Article
- Keywords:
acute myeloid leukemia;
cell viability;
apoptosis
- MeSH:
Humans;
Apoptosis;
Leukemia, Myeloid, Acute/pathology*;
MicroRNAs;
Cell Proliferation;
RNA, Long Noncoding/genetics*;
Cell Movement;
Cell Survival;
Cell Line, Tumor;
HL-60 Cells
- From:
Journal of Experimental Hematology
2025;33(4):998-1006
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the effect of LINC00641 on the viability and apoptosis of acute myeloid leukemia (AML) cells and its mechanism.
METHODS:RT-qPCR was applied to detect the relative expression levels of LINC00641, miR-204-5p, and MT1X in human normal bone marrow stromal cell lines HS-5 and AML cell lines, and to screen the optimal cell line THP-1 was screened for subsequent experiments. Bioinformatics, dual luciferase reporter assay, pull down assay, and RIP assay were applied to validate the targeting relationship between LINC00641, MT1X and miR-204-5p. EdU, CCK-8, flow cytometry, and Transwell assay were applied to detect cell proliferation, apoptosis, migration and invasion, respectively. Western blot was applied to detect the expression of MT1X , CyclinD1, Bcl-2, and Bax proteins.
RESULTS:Compared with HS-5 cells, the expression of LINC00641 and MT1X was obviously increased in HL60, THP-1, U937, and KG1 cells, while the expression of miR-204-5p was obviously reduced (all P <0.05). THP-1 cells showed the most obvious changes (P <0.05). Silencing LINC00641 or overexpressing miR-204-5p was able to obviously inhibit the proliferation, migration and invasion of THP-1 cells, as well as the expression of CyclinD1 and Bcl-2 proteins, while promote cells apoptosis and Bax protein expression (all P <0.05). Bioinformatics analysis, dual luciferase reporter assay, pull down assay, and RIP assay all confirmed that there were targeted relationships between LINC00641, MT1X and miR-204-5p. Inhibiting miR-204-5p or overexpressing MT1X was able to respectively reverse the inhibitory effect of silencing LINC00641 or overexpressing miR-204-5p on THP-1 cells proliferation, migration and invasion, and reduce cells apoptosis.
CONCLUSION:LINC00641 is highly expressed in AML, and inhibition of LINC00641 expression can inhibit cell proliferation, migration, and invasion and increase apoptosis by regulating the miR-204-5p/MT1X axis.
