The oncoprotein HBXIP up-regulates SCG3 through modulating E2F1 and miR-509-3p in hepatoma cells

被引：32

作者：

Wang, Yue ^{[1
]}

Cui, Ming ^{[2
]}

Cai, Xiaoli ^{[1
]}

Sun, Baodi ^{[2
]}

Liu, Fabao ^{[1
]}

Zhang, Xiaodong ^{[2
]}

Ye, Lihong ^{[1
]}

机构：

[1] Nankai Univ, Coll Life Sci, Dept Biochem, State Key Lab Med Chem Biol, Tianjin 300071, Peoples R China

[2] Nankai Univ, Dept Canc Res, Coll Life Sci, State Key Lab Med Chem Biol, Tianjin 300071, Peoples R China

来源：

CANCER LETTERS | 2014年 / 352卷 / 02期

基金：

中国国家自然科学基金;

关键词：

HBXIP; SCG3; E2F1; miR-509-3p; Hepatocellular carcinoma; BREAST-CANCER CELLS; SECRETOGRANIN-III; ANDROGEN DEPRIVATION; OVARIAN-CANCER; LUNG-CANCER; PROLIFERATION; PROTEIN; APOPTOSIS; GENES; DIFFERENTIATION;

D O I：

10.1016/j.canlet.2014.05.007

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Hepatitis B X-interacting protein (HBXIP) is an important oncoprotein in hepatocarcinogenesis. Here, we found that the expression levels of HBXIP were positively associated with those of Secretogranin III (SCG3) in clinical hepatocellular carcinoma tissues. We identified that HBXIP up-regulated the expression of SCG3 through modulating both E2F transcription factor I (E2F1) and miR-509-3p. HBXIP suppressed miR-509-3p through activating NF-kappa B. In function, we showed that SCG3 increased the proliferation of hepatoma cells and HBXIP enhanced the proliferation of the cells via SCG3 in vitro and in vivo. Thus, we conclude that HBXIP facilitates the proliferation of hepatoma cells through up-regulating SCG3. (C) 2014 Elsevier Ireland Ltd. All rights reserved.

引用

页码：169 / 178

页数：10

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