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Biochem Biophys Res Commun. 2014 Dec 12;455(3-4):229-33. doi: 10.1016/j.bbrc.2014.10.153. Epub 2014 Nov 6.

SAMHD1 is down regulated in lung cancer by methylation and inhibits tumor cell proliferation.

Author information

1
Department of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai 200032, China.
2
Department of Thoracic Surgery, The Huadong Hospital, Fudan University, Shanghai 200040, China.
3
Department of Thoracic Surgery, The Huadong Hospital, Fudan University, Shanghai 200040, China. Electronic address: shengxiaoyong_sh@163.com.
4
Department of Thoracic Surgery, The Huadong Hospital, Fudan University, Shanghai 200040, China. Electronic address: WuYun_hd@163.com.

Abstract

The function of dNTP hydrolase SAMHD1 as a viral restriction factor to inhibit the replication of several viruses in human immune cells was well established. However, its regulation and function in lung cancer have been elusive. Here, we report that SAMHD1 is down regulated both on protein and mRNA levels in lung adenocarcinoma compared to adjacent normal tissue. We also found that SAMHD1 promoter is highly methylated in lung adenocarcinoma, which may inhibit its gene expression. Furthermore, over expression of the SAMHD1 reduces dNTP level and inhibits the proliferation of lung tumor cells. These results reveal the regulation and function of SAMHD1 in lung cancer, which is important for the proliferation of lung tumor cells.

KEYWORDS:

Cell proliferation; Lung adenocarcinoma; SAMHD1; dNTP

PMID:
25449277
DOI:
10.1016/j.bbrc.2014.10.153
[Indexed for MEDLINE]

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