IL-6/STAT3 axis initiated CAFs via up-regulating TIMP-1 which was attenuated by acetylation of STAT3 induced by PCAF in HCC microenvironment
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- 作者：Xin Zheng xin.zheng.xjtu@gmail.com" class="auth_mail" title="E-mail the corresponding author ; Meng Xu 987556919@foxmail.com" class="auth_mail" title="E-mail the corresponding author ; Bowen Yao ybwsplendid@126.com" class="auth_mail" title="E-mail the corresponding author ; Cong Wang wangcongwa@126.com" class="auth_mail" title="E-mail the corresponding author ; Yuli Jia 137261184@foxmail.com" class="auth_mail" title="E-mail the corresponding author ; Qingguang Liu ; raymondzhengxin@foxmail.com" class="auth_mail" title="E-mail the corresponding author
- 关键词：HCC ; hepatocellular carcinoma ; IL-6 ; interleukin-6 ; STAT3 ; Signal transducer and activator of transcription 3 ; PCAF ; P300/CBP-associated factor ; HATs ; histone acetyltransferases ; ELISA ; enzyme-linked immunosorbent assay ; Co-IP ; co-immunoprecipitation ; ChIP ; chromatin immunoprecipitation
- 刊名：Cellular Signalling
- 出版年：2016
- 出版时间：September 2016
- 年：2016
- 卷：28
- 期：9
- 页码：1314-1324
- 全文大小：1538 K
文摘
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IL-6/STAT3 signaling was activated aberrantly in HCC tissues and correlated with poor post-surgical outcome.
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IL-6/STAT3 pathway was found to enhance TIMP-1 expression directly via p-STAT3-binding with TIMP-1 promoter in vitro.
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IL-6/STAT3 pathway in HCC cells was shown to induce the transformation from normal LFs to CAFs via up-regulating TIMP-1.
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Co-culture with transformed CAFs promoted the growth of Huh7 cells both in vitro and in vivo.
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PCAF was revealed to acetylate cytoplasmic STAT3 protein directly and regulate TIMP-1 expression negatively in HCC cells.
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