HBXIP up-regulates ACSL1 through activating transcriptional factor Sp1 in breast cancer
HBXIP up-regulates ACSL1 through activating transcriptional factor Sp1 in breast cancer
复制标题
HBXIP 通过激活乳腺癌中的转录因子 Sp1 上调 ACSL1
DOI：
10.1016/j.bbrc.2017.01.126
复制
发表时间：
2017-03-11
影响因子：
3.1
通讯作者：
Ye, Lihong
中科院分区：
文献类型：
--
作者：
Wang, Yue;Cai, Xiaoli;Ye, Lihong
The oncoprotein hepatitis B X-interacting protein (HBXIP) results in the dysregulation of lipid metabolism to enhance the development of breast cancer. Acyl-CoA synthetase long-chain family member 1 (ACSL1) is required for thioesterification of long-chain fatty acids into their acyl-CoA derivatives. In this study, we present a hypothesis that HBXIP might be involved in the regulation of ACSL1 in breast cancer. Interestingly, we found that the overexpression of HBXIP was able to up-regulate ACSL1 at the levels of mRNA and protein in a dose-dependent manner in breast cancer cells. Conversely, silencing of HBXIP led to the opposite results. Mechanistically, HBXIP as a coactivator interacted with transcriptional factor Spl through binding to the promoter of ACSL1 by ChIP assays analysis, leading to the transcription of ACSL1 in breast cancer cells. Immunohistochemistry staining revealed that the positive rate of ACSL1 was 71.4% (35/49) in clinical breast cancer tissues, HBXIP 79.6% (39149), in which the positive rate of ACSL1 was 76.9% (30/39) in the HBXIP-positive specimens. But, few positive rate of ACSL110% (1/10) was observed in normal breast tissues. The mRNA levels of ACSL1 were significantly higher in clinical breast cancer tissues than those in their corresponding peritumor tissues. The mRNA levels of ACSL1 were positively associated with those of HBXIP in clinical breast cancer tissues. Thus, we conclude that the oncoprotein HBXIP is able to up-regulate ACSL1 through activating the transcriptional factor Spl in breast cancer. (C) 2017 Elsevier Inc. All rights reserved.
