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片仔癀抑制miR-483-5p促进的肝癌细胞增殖和干性

Pien Tze Huang Attenuates Cell Proliferation and Stemness Promoted by miR-483-5p in Hepatocellular Carcinoma Cells.

作者信息

Wei Li-Hui, Chen Xi, Shen A-Ling, Fang Yi, Xie Qiu-Rong, Guo Zhi, Sferra Thomas J, Chen You-Qin, Peng Jun

机构信息

Innovation and Transformation Center, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, China.

Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, China.

出版信息

Chin J Integr Med. 2025 May 9. doi: 10.1007/s11655-025-4126-0.

Abstract

OBJECTIVE

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

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

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

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.

摘要

目的

探讨miR-483-5p对肝癌(HCC)细胞增殖和干性的影响,以及片仔癀(PZH)的减弱作用。

方法

通过miRNA微阵列分析鉴定HepG2细胞和肝癌干细胞样细胞(HCSCs)之间差异表达的miRNA。将miR-483-5p模拟物转染到HepG2细胞中,以探讨miR-483-5p对细胞增殖和干性的影响。用PZH(0、0.25、0.50和0.75mg/mL)处理HepG2细胞和HCSCs,以探讨PZH在非诱导状态和miR-483-5p模拟物诱导状态下对增殖和干性的影响。

结果

miR-483-5p在HCSCs中显著上调,其过表达增加了HepG2细胞的增殖和干性(P<0.05)。PZH不仅显著抑制HepG2细胞的增殖,还显著抑制HCSCs的细胞增殖和自我更新(P<0.05)。PZH部分消除了miR-483-5p模拟物对HepG2细胞增殖和干性的影响。

结论

miR-483-5p促进HepG2细胞的增殖并增强其干性,而PZH可减弱这些作用,表明miR-483-5p是治疗HCC的潜在分子靶点,并为PZH用于HCC患者的临床应用提供实验证据。

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