Wei Li-Hui, Chen Xi, Shen A-Ling, Fang Yi, Xie Qiu-Rong, Guo Zhi, Sferra Thomas J, Chen You-Qin, Peng Jun
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.
Chin J Integr Med. 2025 May 9. doi: 10.1007/s11655-025-4126-0.
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).
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.
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.
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.
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。
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。
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。
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。