Effect of DDX5 on the biological function of leukemia K562 cells and its mechanism
10.19405/j.cnki.issn1000-1492.2024.09.010
- VernacularTitle:DDX5对白血病K562细胞生物学功能的影响及其机制
- Author:
Shuang HU
1
;
Xiaoran CHEN
;
Yubin FENG
Author Information
1. 安徽医科大学药学院,合肥 230032
- Keywords:
K562 cells;
DDX5;
cell proliferation;
apoptosis;
cell differentiation;
P53
- From:
Acta Universitatis Medicinalis Anhui
2024;59(9):1557-1563
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of DEAD-box RNA helicases(DDX5 helicase)on the proliferation,apoptosis and differentiation of leukemia cell line K562 cells.Methods Data from the Gene Expression Profiling Interactive Analysis(GEPIA)cancer gene database was utilized to analyze the expression of DDX5 mRNA in tis-sues of leukemia patients.Survival curve analysis was conducted to assess the relationship between DDX5 mRNA expression levels and the prognosis of leukemia patients.Small interfering RNA(siRNA)was used for transient transfection of K562 cells to knock down DDX5.Real-time quantitative PCR(RT-PCR)was employed to verify the silencing effect,and Western blot was used to detect protein expression levels.CCK-8 assay was conducted to ex-amine cell proliferation capability,and Western blot and immunofluorescence were utilized to detect the expression levels of cell proliferation-related proteins.Flow cytometry was used to detect cell apoptosis,and the expression lev-els of cell differentiation-related proteins were assessed by flow cytometry and Western blot.Lastly,the effects of DDX5 silencing on the expression levels of P21 and P53 proteins were examined by RT-PCR and Western blot.Re-sults GEPIA database analysis revealed that the expression level of DDX5 in human leukemia bone marrow tissues was significantly higher than that in healthy individuals,and patients with low DDX5 expression had longer survival time.In vitro experiments demonstrated that knocking down DDX5 significantly inhibited the proliferation of K562 cells.Flow cytometry results indicated that DDX5 silencing promoted apoptosis and induced cell differentiation by enhancing the expression of CD11b and CD14 proteins.Furthermore,silencing DDX5 up-regulated the expression levels of P21 and P53 proteins.Conclusion DDX5 may potentially inhibit the proliferation of leukemia cell line K562,promote apoptosis,and induce differentiation by targeting P53.
