机构：[1]Hongqiao Institute of Medicine, Tongren Hospital/Faculty of Basic Medicine, Shanghai Jiaotong University School of Medicine, Shanghai, China[2]Shanghai Key Laboratory forTumor Microenvironment and Inflammation, Department of Biochemistry & Molecular Cellular Biology, Shanghai Jiaotong University School of Medicine, Shanghai, China[3]KeyLaboratory of Computational Biology, CAS-MPG Partner Institute of Computational Biology, Shanghai Institute for Biological Science, Chinese Academy of Sciences, Shanghai,China[4]Digestive Endoscopy Center, Shanghai Tongren Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China[5]Naruiboen Biomedical TechnologyCorporation Limited, Linyi, Shandong, China[6]Shandong Provincial Hospital, Shandong Laboratory Animal Center, Science and Technology Innovation Center, Shandong FirstMedical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China[7]Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education,Shanghai, China[8]Linyi University-Shanghai Jiaotong University Joint Institute of Translational Medicine, Linyi, Shandong, China
The transcriptional repressor Snail induces EMT during embryonic development and tumor metastasis. Growing evidence indicates that Snail functions as a trans-activator to induce gene expression; however, the underlying mechanism remains elusive. Here, we report that Snail cooperates with GATA zinc finger protein p66 & beta; to transactivate genes in breast cancer cells. Biologically, depletion of p66 & beta; reduces cell migration and lung metastasis in BALB/c mice. Mechanistically, Snail interacts with p66 & beta; and cooperatively induces gene transcription. Notably, a group of genes induced by Snail harbor conserved G-rich cis-elements (5 & PRIME;-GGGAGG-3 & PRIME;, designated as G-box) in their proximal promoter regions. Snail directly binds to G-box via its zinc fingers and transactivates the G-box-containing promoters. p66 & beta; enhances Snail binding affinity to G-box, whereas depletion of p66 & beta; results in a decreased binding affinity of Snail to the endogenous promoters and concomitantly reduces the transcription of Snail-induced genes. Taken together, these data demonstrated that p66 & beta; is critical for Snail-mediated cell migration by acting as a co-activator of Snail to induce genes containing G-box elements in the promoters.
第一作者机构：[1]Hongqiao Institute of Medicine, Tongren Hospital/Faculty of Basic Medicine, Shanghai Jiaotong University School of Medicine, Shanghai, China[2]Shanghai Key Laboratory forTumor Microenvironment and Inflammation, Department of Biochemistry & Molecular Cellular Biology, Shanghai Jiaotong University School of Medicine, Shanghai, China
共同第一作者：
通讯作者：
通讯机构：[1]Hongqiao Institute of Medicine, Tongren Hospital/Faculty of Basic Medicine, Shanghai Jiaotong University School of Medicine, Shanghai, China[2]Shanghai Key Laboratory forTumor Microenvironment and Inflammation, Department of Biochemistry & Molecular Cellular Biology, Shanghai Jiaotong University School of Medicine, Shanghai, China[7]Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education,Shanghai, China[8]Linyi University-Shanghai Jiaotong University Joint Institute of Translational Medicine, Linyi, Shandong, China
推荐引用方式(GB/T 7714)：
Zou Xiuqun,Ma Li,Zhang Yihong,et al.GATA zinc finger protein p66 & beta; promotes breast cancer cell migration by acting as a co-activator of Snail[J].CELL DEATH & DISEASE.2023,14(6):doi:10.1038/s41419-023-05887-w.
APA：
Zou, Xiuqun,Ma, Li,Zhang, Yihong,Zhang, Qun,Xu, Chu...&Jia, Hao.(2023).GATA zinc finger protein p66 & beta; promotes breast cancer cell migration by acting as a co-activator of Snail.CELL DEATH & DISEASE,14,(6)
MLA：
Zou, Xiuqun,et al."GATA zinc finger protein p66 & beta; promotes breast cancer cell migration by acting as a co-activator of Snail".CELL DEATH & DISEASE 14..6(2023)
生物学