CXXC5 suppresses hepatocellular carcinoma by promoting TGF-beta-induced cell cycle arrest and apoptosis
文献类型：期刊论文
| 作者 | Yan, Xiaohua1,2; Wu, Jingyi1; Chen, Ye-Guang1; Jiang, Quanlong3; Cheng, Hao3; Han, Jing-Dong J.3; , |
| 刊名 | JOURNAL OF MOLECULAR CELL BIOLOGY
 |
| 出版日期 | 2018 |
| 卷号 | 10期号:1页码:48-59 |
| 关键词 | hepatocellular carcinoma (HCC) TGF-beta CXXC5 HDAC signaling regulation |
| ISSN号 | 1674-2788 |
| DOI | 10.1093/jmcb/mjx042 |
| 文献子类 | Article |
| 英文摘要 | Evading TGF-beta-mediated growth inhibition is often associated with tumorigenesis in liver, including hepatocellular carcinoma (HCC). To better understand the functions and the underlying molecular mechanisms of TGF-beta in HCC initiation and progression, we carried out transcriptome sequencing (RNA-Seq) to identify the target genes of TGF-beta. CXXC5, a member of the CXXC-type zinc finger domain-containing protein family, was identified as a novel TGF-beta target gene in Hep3B HCC cells. Knockdown of CXXC5 attenuated the expression of a substantial portion of TGF-beta target genes and ameliorated TGF-beta-induced growth inhibition or apoptosis of Hep3B cells, suggesting that CXXC5 is required for TGF-beta-mediated inhibition of HCC progression. Analysis of the TCGA database indicated that CXXC5 expression is reduced in the majority of HCC tissue samples in comparison to that in normal tissues. Furthermore, CXXC5 associates with the histone deacetylase HDAC1 and competes its interaction with Smad2/3, thereby abolishing the inhibitory effect of HDAC1 on TGF-beta signaling. These observations together suggest that CXXC5 may act as a tumor suppressor by promoting TGF-beta signaling via a positive feedback loop, and reveal a strategy for HCC to bypass TGF-beta-mediated cytostasis by disrupting the positive feedback regulation. Our findings shed new light on TGF-beta signaling regulation and demonstrate the function of CXXC5 in HCC development. |
| 学科主题 | Cell Biology |
| WOS关键词 | TRANSFORMING-GROWTH-FACTOR ; ACUTE MYELOID-LEUKEMIA ; TARGET GENE ; CANCER ; DIFFERENTIATION ; INHIBITION ; RECEPTOR ; SMAD7 ; LIVER ; EXPRESSION |
| 语种 | 英语 |
| WOS记录号 | WOS:000428634600005 |
| 出版者 | OXFORD UNIV PRESS |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.144/handle/331004/1023]  |
| 专题 | 中国科学院上海生命科学研究院营养科学研究所 |
| 作者单位 | 1.Tsinghua Univ, Sch Life Sci, Tsinghua Peking Ctr Life Sci, State Key Lab Membrane Biol, Beijing 100084, Peoples R China; 2.Nanchang Univ, Sch Basic Med Sci, Dept Biochem & Mol Biol, Nanchang 330006, Jiangxi, Peoples R China; 3.Chinese Acad Sci, Shanghai Inst Biol Sci, Max Planck Partner Inst Computat Biol, Shanghai 200031, Peoples R China, |
| 推荐引用方式 GB/T 7714 | Yan, Xiaohua,Wu, Jingyi,Chen, Ye-Guang,et al. CXXC5 suppresses hepatocellular carcinoma by promoting TGF-beta-induced cell cycle arrest and apoptosis[J]. JOURNAL OF MOLECULAR CELL BIOLOGY,2018,10(1):48-59. |
| APA | Yan, Xiaohua.,Wu, Jingyi.,Chen, Ye-Guang.,Jiang, Quanlong.,Cheng, Hao.,...&,.(2018).CXXC5 suppresses hepatocellular carcinoma by promoting TGF-beta-induced cell cycle arrest and apoptosis.JOURNAL OF MOLECULAR CELL BIOLOGY,10(1),48-59. |
| MLA | Yan, Xiaohua,et al."CXXC5 suppresses hepatocellular carcinoma by promoting TGF-beta-induced cell cycle arrest and apoptosis".JOURNAL OF MOLECULAR CELL BIOLOGY 10.1(2018):48-59. |
入库方式： OAI收割
来源：上海营养与健康研究所
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