Effects of Down-regulation of NCL Expression on the Biological Behavior of Acute Myeloid Leukemia Kasumi-1 Cells.
10.19746/j.cnki.issn.1009-2137.2025.05.012
- Author:
Hui-Li LIU
1
;
Wen-Xin XU
1
;
Yang-Yan CAI
1
;
Hong-Mei LI
1
Author Information
1. Department of Medical Technology, Zhangzhou Health Vocational College, Collaborative Innovation Center for Translation Medical Testing and Application Technology Zhangzhou, Zhangzhou 363000, Fujian Province, China.
- Publication Type:Journal Article
- Keywords:
nucleolin;
acute myeloid leukemia;
TP53-CDKN1A pathway
- MeSH:
Humans;
Leukemia, Myeloid, Acute/pathology*;
Down-Regulation;
Cell Proliferation;
Apoptosis;
RNA-Binding Proteins/genetics*;
Nucleolin;
Cell Line, Tumor;
Phosphoproteins/metabolism*;
Cell Cycle;
Signal Transduction;
RNA, Small Interfering
- From:
Journal of Experimental Hematology
2025;33(5):1312-1317
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the role of nucleolin (NCL) in acute myeloid leukemia (AML) Kasumi-1 cells and its underlying mechanism.
METHODS:The Kasumi-1 cells were infected with lentivirus carrying shRNA to downregulate NCL expression. Cell proliferation was detected by CCK-8 assay, and cell apoptosis and cell cycle were determined by flow cytometry. Transcriptome next-generation sequencing (NGS) was performed to predict associated signaling pathways, the expression levels of related genes were measured by RT-PCR.
RESULTS:Down-regulation of NCL expression significantly inhibited the proliferation of Kasumi-1 cells (P <0.01) and markedly increased the apoptosis rate (P <0.001). Cell cycle analysis showed significant changes in the distribution of cells in the G1 and S phases after NCL knockdown (P <0.05), while no significant difference was observed in the G2 phase (P >0.05). Transcriptome sequencing analysis demonstrated that differentially expressed genes in Kasumi-1 cells with low expression of NCL were primarily enriched in key signaling pathways, including ribosome, spliceosome, RNA transport, cell cycle, and amino acid biosynthesis. qPCR validation showed that the expression of BAX, CASP3, CYCS, PMAIP1, TP53 , and CDKN1A was significantly upregulated after NCL downregulation (P <0.05), with CDKN1A exhibiting the most pronounced difference.
CONCLUSION:NCL plays a critical role in regulating the proliferation, apoptosis, and cell cycle progression of Kasumi-1 cells. The mechanism likely involves suppressing cell cycle progression through activation of the TP53-CDKN1A pathway and promoting apoptosis by upregulating apoptosis-related genes.
