机构：[1]Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academyof Sciences, Kunming, China[2]Department of Biology, Yuxi Normal University, Yuxi, China[3]University of the Chinese Academy of Sciences, Beijing, China[4]Department ofBiochemistry and Molecular Biology, Kunming Medical University, Kunming, China[5]Department of Pathology, First Affiliated Hospital of Kunming Medical University, Kunming,China医技科室病理科昆明医科大学附属第一医院[6]Cancer Hospital, Kunming Medical University, Kunming, China[7]Department of Laboratory Medicine & Central Laboratory, Southern Medical University-AffiliatedFengxian Hospital, Shanghai, Chin
The Kruppel-like factor 5 (KLF5) transcription factor is highly expressed in high-grade and basal-like breast cancers. However, the mechanism by which KLF5 promotes cell migration and invasion is still not completely understood. In this study, we demonstrate that TNFAIP2, a tumor necrosis factor-alpha (TNF alpha)-induced gene, is a direct KLF5 target gene. The expression of TNFAIP2 is highly correlated with the expression of KLF5 in breast cancers. The manipulation of KLF5 expression positively alters TNFAIP2 expression levels. KLF5 directly binds to the TNFAIP2 gene promoter and activates its transcription. Functionally, KLF5 promotes cancer cell proliferation, migration and invasion in part through TNFAIP2. TNFAIP2 interacts with the two small GTPases Rac1 and Cdc42, thereby increasing their activities to change actin cytoskeleton and cell morphology. These findings collectively suggest that TNFAIP2 is a direct KLF5 target gene, and both KLF5 and TNFAIP2 promote breast cancer cell proliferation, migration and invasion through Rac1 and Cdc42.
基金：
Strategic Priority Research Program of the Chinese Academy of Sciences, Stem Cell and Regenerative Medicine Research [XDA01040406]; National Natural Science Foundation of ChinaNational Natural Science Foundation of China [81120108019, 81325016, U1132605, 81322038, 81272930]; West Light Foundation of Chinese Academy of SciencesChinese Academy of Sciences; Shanghai Health System outstanding academic leader training program [XBR2013114]
第一作者机构：[1]Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academyof Sciences, Kunming, China[2]Department of Biology, Yuxi Normal University, Yuxi, China[3]University of the Chinese Academy of Sciences, Beijing, China
通讯作者：
通讯机构：[*1]Department of Laboratory Medicine & Central Laboratory, Southern Medical University-Affiliated Fengxian Hospital, Shanghai 201499, China[*2]Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, 32 Jiaochang East Road, Kunming, 650223 Yunnan, China
推荐引用方式(GB/T 7714)：
Jia L.,Zhou Z.,Liang H.,et al.KLF5 promotes breast cancer proliferation, migration and invasion in part by upregulating the transcription of TNFAIP2[J].ONCOGENE.2016,35(16):2040-2051.doi:10.1038/onc.2015.263.
APA：
Jia, L.,Zhou, Z.,Liang, H.,Wu, J.,Shi, P....&Chen, C..(2016).KLF5 promotes breast cancer proliferation, migration and invasion in part by upregulating the transcription of TNFAIP2.ONCOGENE,35,(16)
MLA：
Jia, L.,et al."KLF5 promotes breast cancer proliferation, migration and invasion in part by upregulating the transcription of TNFAIP2".ONCOGENE 35..16(2016):2040-2051
医学