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| 1 | Structural insights into the TRIM family of ubiquitin E3 ligases显示文摘 | Yang Li Han Wu Wei Wu Wei Zhuo Weixiao Liu Yixiao Zhang Minzhang Cheng Ye-Guang Chen Ning Gao Hongtao Yu Linfang Wang Wei Li Maojun Yang | 2014 | Cell Research2014，24，6： | 12 |
| 2 | Yin Yang 1(YY1) synergizes with Smad7 to inhibit TGF-β signaling in the nucleus显示文摘As a prototype of the TGF-βsuperfamily cytokines,TGF-βis well known for its diverse roles in embryogenesis and adult tissue homeostasis.TGF-βevokes cellular responses by signaling mainly through cell membrane receptors and transcription factor R-Smads and Co-Smad(Smad4),while an inhibitory Smad,Smad7,acts as a critical negative regulator of TGF-βsignaling.Smad7 antagonizes TGF-βsignaling by regulating the stability or activity of the receptors or blocking the DNA binding of the functional R-Smad-Smad4 complex in the nucleus.However,the function of Smad7 in the nucleus is not fully understood.Yin Yang 1(YY1)is a ubiquitously expressed transcription factor with multiple functions.It has been reported that YY1 can inhibit Smad-dependent transcriptional responses and TGF-β/BMP-induced cell differentiation independently of its DNA binding ability.In this study,we found that Smad7 interacts with YY1 and the interaction is attenuated by TGF-βsignaling.Reporter assays and target gene expression analyses revealed that Smad7 and YY1 act in concert to inhibit TGF-β-induced transcription in the nucleus.Furthermore,Smad7 could enhance the interaction of YY1 with the histone deacetylase HDAC1.Consistently,YY1 and HDAC1 augmented the transcription repression activity of Smad7 in Gal4-luciferase reporter analysis.Therefore,our findings define a novel mechanism of Smad7 and YY1 to antagonize TGF-βsignaling. | YAN XiaoHua PAN Jun XIONG WanWan CHENG MinZhang SUN YingYuan ZHANG SuPing CHEN YeGuang | 2014 | Science China(Life Sciences)2014，57，1： | 10 |
| 3 | Tea domain transcription factor TEAD4 mitigatesTGF-β signaling and hepatocellular carcinomaprogression independently of YAP显示文摘Tea domain transcription factor 4 (TEAD4) plays a pivotal role in tissue development and homeostasis by interacting with Yesassociated protein (YAP) in response to Hippo signaling inactivation. TEAD4 and YAP can also cooperate with transforminggrowth factor-β (TGF-β)-activated Smad proteins to regulate gene transcription. Yet, it remains unclear whether TEAD4 playsa YAP-independent role in TGF-β signaling. Here, we unveil a novel tumor suppressive function of TEAD4 in liver cancer viamitigating TGF-β signaling. Ectopic TEAD4 inhibited TGF-β-induced signal transduction, Smad transcriptional activity, and targetgene transcription, consequently suppressing hepatocellular carcinoma cell proliferation and migration in vitro and xenografttumorgrowth in mice. Consistently, depletion of endogenous TEAD4 by siRNAs enhanced TGF-β signaling in cancer cells. Mechanistically,TEAD4 associates with receptor-regulated Smads (Smad2/3) and Smad4 in the nucleus, thereby impairing the binding of Smad2/3to the histone acetyltransferase p300. Intriguingly, these negative effects of TEAD4 on TGF-β/Smad signaling are independent ofYAP, as impairing the TEAD4–YAP interaction through point mutagenesis or depletion of YAP and/or its paralog TAZ has little effect.Together, these results unravel a novel function of TEAD4 in fine tuning TGF-β signaling and liver cancer progression in a YAPindependent manner. | Weicheng Luo Yi Li Yi Zeng Yining Li Minzhang Cheng Cheng Zhang Fei Li Yiqing Wu Chunhong Huang Xiaolong Yang Joachim Kremerskothen Jianmin Zhang Chunbo Zhang Shuo Tu Zhihua Li Zhijun Luo Zhenghong Lin Xiaohua Yan | 2023 | Journal of Molecular Cell Biology2023，15，2： | 0 |
| 4 | Aberrant expression of the extracellular matrix component Biglycan regulated by Hedgehog signalling promotes colorectal cancer cell proliferation显示文摘Hedgehog(Hh)signalling plays essential roles in regulating embryonic development and contributes to tumour initiation,growth and progression in multiple cancers.The detailed mechanism by which Hh signalling participates in tumour growth warrants thorough study,although several downstream target genes have been identified.Herein,a set of novel targets of Hh signalling was identified in multiple types of tumour cells via RNA-Seq analysis.Among these targets,the expression regulation and oncogenic function of the extracellular matrix component biglycan(BGN)were investigated.Further investigation verified that Hh signalling activates the expression of BGN via the transcription factor Gli2,which directly binds to the promoter region of BGN.Functional assays revealed that BGN facilitates tumour cell growth and proliferation in colorectal cancer(CRC)cells,and xenograft assays confirmed that BGN also promotes tumour growth in vivo.Moreover,analysis of clinical CRC samples showed that both the protein and mRNA levels of BGN are increased in CRC tissues compared to those in adjacent tissues,and higher expression of BGN is correlated with poorer prognosis of CRC patients,further confirming the function of BGN in CRC.Taken together,aberrantly activated Hh signalling increases the expression of BGN,possibly regulates the extracellular matrix,and thereby promotes tumour growth in CRC. | Shaopeng Zeng Feifei Zhou Yiqing Wang Zhenyu Zhai Linlin Xu Hailong Wang Xinping Chen Shiwen Luo Minzhang Cheng | 2022 | Acta Biochimica et Biophysica Sinica2022，54，2： | 0 |
| 5 | ATF1 promotes the malignancy of lung adenocarcinoma cells by transcriptionally regulating ZNF143 expression显示文摘The clinical oncogenic functions and mechanisms of activating transcription factor 1(ATF1)in the progression of lung adenocarcinoma have not been completely elucidated.In this study,by employing human lung adenocarcinoma tissues and cells,we detect the correlation of ATF1 expression with the clinicopathological features and prognosis of patients with lung adenocarcinoma and find that ATF1 promotes lung adenocarcinoma cell proliferation and migration by transcriptionally enhancing zinc finger protein 143(ZNF143)expression.ATF1 and ZNF143 are strongly expressed in lung adenocarcinoma tissues compared with those in the adjacent normal tissues,and high ATF1 and ZNF143 expressions are related to poor disease-free survival of lung adenocarcinoma patients.ATF1 overexpression results in increased proliferation and migration of lung adenocarcinoma cells,whereas knockdown of ATF1 inhibits cell proliferation and migration.Furthermore,ATF1 transcriptionally regulates the expression of ZNF143,and ATF1 and ZNF143 expressions are positively correlated in lung adenocarcinoma tissues.ZNF143 knockdown blocks lung adenocarcinoma cell migration,which is mediated by ATF1 upregulation.Hence,this study provides a potential therapeutic candidate for the treatment of lung adenocarcinoma. | Jinhong Mei Yu Liu Yiyun Sheng Ying Liu Limin Chen Hailong Wang Minzhang Cheng Zhenyu Zhai Linlin Xu | 2023 | Acta Biochimica et Biophysica Sinica2023，55，5： | 0 |
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