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Effects of nitric oxide on the biological behavior of HepG2 human hepatocellular carcinoma cells

机译:一氧化氮对人肝癌细胞HepG2生物学行为的影响

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摘要

Many studies have found the function of nitric oxide (NO) in cancer as a pro-neoplastic vs. an anti-neoplastic effector, but the role of NO in hepatocellular carcinoma (HCC) remains unclear. The present study aimed to investigate the effects of nitric oxide (NO) on the biological behavior of the human hepatocellular carcinoma cell line HepG2. HepG2 cell was cultured in vitro and treated with or without sodium nitroprusside (SNP), a NO donor. Subsequently, we evaluated the effects of NO in cell proliferation, cell cycle, apoptosis, migration and invasion by MTT assay, flow cytometry, wound healing assay and Matrigel invasion assay. We demonstrate that NO significantly inhibited HepG2 cell proliferation by inducing G0/G1 phase arrest in a dose-dependent manner. In addition, compared to the control group, cells treated with SNP showed obviously higher apoptosis ratios in a dose-dependent manner. Furthermore, we revealed that NO effectively inhibited the ability of migration and invasion of HepG2 cells. Taken together, our results suggested that NO has an important role in the regulation of biological behavior in HepG2 cells and the potential for use in the prevention and treatment of HCC.
机译:许多研究发现一氧化氮(NO)在癌症中的作用是促肿瘤作用与抗肿瘤作用的作用,但NO在肝细胞癌(HCC)中的作用仍不清楚。本研究旨在调查一氧化氮(NO)对人肝癌细胞株HepG2生物学行为的影响。体外培养HepG2细胞,并用或不用NO供体硝普钠(SNP)处理。随后,我们通过MTT测定,流式细胞术,伤口愈合测定和Matrigel侵袭测定评估了NO对细胞增殖,细胞周期,凋亡,迁移和侵袭的影响。我们证明,NO通过以剂量依赖的方式诱导G0 / G1期停滞来显着抑制HepG2细胞增殖。另外,与对照组相比,用SNP处理的细胞以剂量依赖性方式显示出明显更高的凋亡率。此外,我们发现,NO可以有效抑制HepG2细胞的迁移和侵袭能力。综上所述,我们的结果表明,NO在调节HepG2细胞的生物学行为中具有重要作用,并且在预防和治疗HCC中具有潜在的作用。

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