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DNM3通过激活P53抑制肝细胞癌生长。

DNM3 Attenuates Hepatocellular Carcinoma Growth by Activating P53.

作者信息

Zhang Zhengdong, Chen Chun, Guo Weike, Zheng Shengbao, Sun Zhenghua, Geng Xiaoping

机构信息

Department of General Surgery, The Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China (mainland).

0.

出版信息

Med Sci Monit. 2016 Jan 19;22:197-205. doi: 10.12659/msm.896545.

DOI:10.12659/msm.896545
PMID:26784388
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4725618/
Abstract

BACKGROUND

Primary hepatocellular carcinoma is one of the most common malignant tumors in China and its mortality rate shows no sign at present of ceasing to rise. In our previous study, we found that the mRNA level of Dynamin3 (DNM3), a member of the Dynamin family, is significantly lower in hepatocellular carcinoma tissues than in non-tumor tissues. The aim of this study was to investigate the expression pattern and potential function of DNM3 in hepatocellular carcinoma.

MATERIAL/METHODS: First, we determined the expression ofDNM3 in human hepatocellular carcinoma tissues and cell lines. We then studied the biological function of DNM3 on hepatocellular carcinoma cells by proliferation assay and colony formation assay. Flow cytometry was used to study the effect of DNM3 on cell cycle and apoptosis.

RESULTS

Expression of DNM3 was significantly downregulated in hepatocellular carcinoma tissues and was associated with vein invasion and tumor metastasis. In addition, upregulation of DNM3 reduced hepatocellular carcinoma cell proliferation and colony formation, induced hepatocellular carcinoma cell G0/G1 phase arrest, and stimulated hepatocellular carcinoma cell apoptosis. We also found that DNM3 may exert its anti-proliferative effect through upregulating p53.

CONCLUSIONS

Our findings suggest that DNM3 attenuates the proliferation and induces apoptosis of gastric cancer cells. Modulation of DNM3 may prove to be an efficient method of hepatocellular carcinoma treatment.

摘要

背景

原发性肝细胞癌是中国最常见的恶性肿瘤之一，目前其死亡率仍呈上升趋势。在我们之前的研究中，我们发现发动蛋白家族成员发动蛋白3（DNM3）的mRNA水平在肝癌组织中显著低于非肿瘤组织。本研究旨在探讨DNM3在肝癌中的表达模式及潜在功能。

材料/方法：首先，我们检测了DNM3在人肝癌组织和细胞系中的表达。然后，我们通过增殖实验和集落形成实验研究了DNM3对肝癌细胞的生物学功能。采用流式细胞术研究DNM3对细胞周期和凋亡的影响。

结果

DNM3在肝癌组织中的表达显著下调，且与静脉侵犯和肿瘤转移相关。此外，上调DNM3可降低肝癌细胞增殖和集落形成，诱导肝癌细胞G0/G1期阻滞，并刺激肝癌细胞凋亡。我们还发现DNM3可能通过上调p53发挥其抗增殖作用。

结论

我们的研究结果表明，DNM3可减弱肝癌细胞的增殖并诱导其凋亡。调节DNM3可能是一种有效的肝癌治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2743/4725618/cd6b8fda435d/medscimonit-22-197-g006.jpg
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