
FOLLOWUS
1.Innovation and Transformation Center, Fujian University of Traditional Chinese Medicine, Fuzhou (350122), China
2.Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou (350122), China
3.Fujian Key Laboratory of Integrative Medicine in Geriatrics, Fujian University of Traditional Chinese Medicine, Fuzhou (350122), China
4.Department of Oncology, the 900th Hospital of the Chinese People's Liberation Army Joint Service Support Force, Fuzhou (350003), China
5.Department of Pediatrics, Rainbow Babies and Children's Hospital and Case Western Reserve University School of Medicine, Cleveland, OH (44106), USA
Prof. PENG Jun, E-mail: pjunlab@hotmail.com
录用日期:2024-09-11,
网络出版日期:2025-05-05,
纸质出版日期:2025-09
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片仔癀通过miR-483-5p抑制肝癌细胞增殖和干性[J]. 中国结合医学杂志(英文版), 2025,31(9):782-791.
WEI Li-hui, CHEN Xi, SHEN A-ling, et al. Pien Tze Huang Attenuates Cell Proliferation and Stemness Promoted by miR-483-5p in Hepatocellular Carcinoma Cells[J]. Chinese journal of integrative medicine, 2025, 31(9): 782-791.
片仔癀通过miR-483-5p抑制肝癌细胞增殖和干性[J]. 中国结合医学杂志(英文版), 2025,31(9):782-791. DOI: 10.1007/s11655-025-4126-0.
WEI Li-hui, CHEN Xi, SHEN A-ling, et al. Pien Tze Huang Attenuates Cell Proliferation and Stemness Promoted by miR-483-5p in Hepatocellular Carcinoma Cells[J]. Chinese journal of integrative medicine, 2025, 31(9): 782-791. DOI: 10.1007/s11655-025-4126-0.
目的:
2
探讨 miR-483-5p 对肝癌细胞增殖与干性的影响
以及片仔癀的抑制作用.
方法:
2
通过 miRNA 微阵列分析鉴定HepG2细胞与肝癌干细胞样细胞 (Hepatic cancer stem-like cells
HCSCs) 间差异表达的miRNA. 将miR-483-5p mimics转染至HepG2细胞
探究其过表达对细胞增殖与干性的调控作用. 采用不同浓度片仔癀 (0 mg/mL、0.25 mg/mL、0.50 mg/mL、0.75 mg/mL) 处理 HepG2 细胞及HCSCs
评估miR-483-5p过表达对细胞增殖与干性的影响.
结果:
2
与HepG2细胞比较
miR-483-5p在HCSCs中显著上调 (
P
<
0.05) ; miR-483-5p过表达可促进HepG2细胞增殖
并增强干性; 片仔癀干预后显著抑制HepG2细胞的增殖
并有效抑制HCSCs的增殖与自我更新能力 (
P
<
0.05) ; 片仔癀可部分消除miR-483-5p过表达后对HepG2细胞增殖与干性的促进作用.
结论:
2
miR-483-5p通过增强肝癌细胞增殖与干性促进肿瘤进展
而片仔癀能有效抑制这一过程
表明 miR-483-5p 是肝癌治疗的潜在靶点
同时为片仔癀的临床应用提供了实验依据.
Objective:
2
To investigate the effect of miR-483-5p on hepatocellular carcinoma (HCC) cells proliferation and stemness
as well as the attenuating effect of Pien Tze Huang (PZH).
Methods:
2
Differentially expressed miRNA between HepG2 cells and hepatic cancer stem-like cells (HCSCs) were identified by a miRNA microarray assay. miR-483-5p mimics were transfected into HepG2 cells to explore the effects of miR-483-5p on cell proliferation and stemness. HepG2 cells and HCSCs were treated with PZH (0
0.25
0.50 and 0.75 mg/mL) to explore the effects of PZH on the proliferation and stemness
both in non-induced state and the state induced by miR-483-5p mimics.
Results:
2
miR-483-5p was significantly up-regulated in HCSCs and its overexpression increased cell proliferation and stemness in HepG2 cells (
P
<
0.05). PZH not only significantly inhibited proliferation in HepG2 cells
but also significantly suppressed the cell proliferation and self-renewal of HCSCs (
P
<
0.05). The effects of miR-483-5p mimics on proliferation and stemness of HepG2 cells were partially abolished by PZH.
Conclusions:
2
miR-483-5p promotes proliferation and enhances stemness of HepG2 cells
which were attenuated by PZH
demonstrating that miR-483-5p is a potential molecular target for the treatment of HCC and provide experimental evidence to support clinical use of PZH for patients with HCC.
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