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灵芝酸 A 抑制人肝癌细胞的增殖、侵袭,促进其凋亡。

Ganoderic acid A inhibits proliferation and invasion, and promotes apoptosis in human hepatocellular carcinoma cells.

机构信息

Department of Colorectal and Anal Surgery, The First Hospital, Jilin University, Changchun, Jilin 130000, P.R. China.

出版信息

Mol Med Rep. 2017 Oct;16(4):3894-3900. doi: 10.3892/mmr.2017.7048. Epub 2017 Jul 21.

Abstract

Ganoderic acid A (GA‑A), a triterpenoid, has been demonstrated to suppress cell proliferation in various cancers, including breast cancer and osteosarcoma. However, its effect on human hepatocellular carcinoma (HCC) remains to be elucidated. The present study aimed to investigate the effect of GA‑A on HCC cells in vitro. The HepG2 and SMMC7721 human HCC cell lines were treated with differing concentrations of GA‑A for 24, 48 and 72 h. The cell growth rate, cell cycle and apoptosis, migration and invasion were determined using a Cell Counting Kit‑8, flow cytometry and transwell assays, respectively. The expression of apoptosis‑associated proteins was detected via western blot analysis. GA‑A significantly inhibited the proliferation of human HCC HepG2 and SMMC7721 cells in a dose‑dependent manner. Furthermore, GA‑A induced cell cycle arrest at the G0/G1 phase and apoptosis, and suppressed the migration and invasion of HCC cells. Furthermore, GA‑A decreased the expression of cyclin D1 and increased the expression of p21 and cleaved caspase‑3. In conclusion, GA‑A suppressed the proliferation of human HCC cells in vitro and may act as a promising natural therapeutic reagent in the treatment of HCC.

摘要

灵芝酸 A(GA-A)是一种三萜类化合物,已被证明可抑制多种癌症(包括乳腺癌和骨肉瘤)的细胞增殖。然而,其对人肝癌(HCC)的影响仍有待阐明。本研究旨在探讨 GA-A 对 HCC 细胞的体外作用。用不同浓度的 GA-A 处理 HepG2 和 SMMC7721 人 HCC 细胞系 24、48 和 72 h。使用细胞计数试剂盒-8、流式细胞术和 Transwell 测定分别确定细胞生长速率、细胞周期和凋亡、迁移和侵袭。通过 Western blot 分析检测凋亡相关蛋白的表达。GA-A 以剂量依赖性方式显著抑制人 HCC HepG2 和 SMMC7721 细胞的增殖。此外,GA-A 诱导细胞周期停滞在 G0/G1 期并诱导细胞凋亡,并抑制 HCC 细胞的迁移和侵袭。此外,GA-A 降低了细胞周期蛋白 D1 的表达,增加了 p21 和 cleaved caspase-3 的表达。综上所述,GA-A 抑制了人 HCC 细胞的体外增殖,可能作为 HCC 治疗的一种有前途的天然治疗试剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d37/5646967/6c1b0b9d30e2/MMR-16-04-3894-g00.jpg

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