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论文题目: Hypermethylated in cancer 1(HIC1) suppresses non-small cell lung cancer progression by targeting interleukin-6/Stat3 pathway
英文论文题目: Hypermethylated in cancer 1(HIC1) suppresses non-small cell lung cancer progression by targeting interleukin-6/Stat3 pathway
第一作者: Wang, XM; Wang, YY; Xiao, G; Wang, JL; Zu, LD; Hao, MG; Sun, XQ; Fu, YJ; Hu, GH; Wang, JH
英文第一作者: Wang, XM; Wang, YY; Xiao, G; Wang, JL; Zu, LD; Hao, MG; Sun, XQ; Fu, YJ; Hu, GH; Wang, JH
联系作者: Wang, JH (reprint author), Fudan Univ, Inst Canc, Shanghai Canc Ctr, Shanghai 200433, Peoples R China.
英文联系作者: Wang, JH (reprint author), Fudan Univ, Inst Canc, Shanghai Canc Ctr, Shanghai 200433, Peoples R China.
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发表年度: 2016
卷: 7
期: 21
页码: 30350-30364
摘要: Non-small cell lung cancer (NSCLC), which accounts for more than 80% of lung cancers, is a leading cause of cancer mortality worldwide. However, the mechanism underlying its progression remains unclear. Here we found that HIC1 promoter was heavily methylated in NSCLC cell lines and tissues contributing to its low expression compared to normal controls. Restoring HIC1 expression inhibited migration, invasion and promoted inducible apoptosis of NSCLC cells. Notably, HIC1 is a tumor suppressor through inhibiting the transcription of IL-6 by sequence-specific binding on its promoter. Restoring IL-6 expression could partially rescue these phenotypes induced by HIC1 in vitro and in vivo. Mechanistic analyses show that autocrine secretion of IL-6 induced by loss of HIC1 activated STAT3 through IL-6/JAK pathway and was associated with NSCLC progression. The HIC1/IL-6 axis may serve as a prognostic biomarker and provide an attractive therapeutic target for NSCLC.
英文摘要: Non-small cell lung cancer (NSCLC), which accounts for more than 80% of lung cancers, is a leading cause of cancer mortality worldwide. However, the mechanism underlying its progression remains unclear. Here we found that HIC1 promoter was heavily methylated in NSCLC cell lines and tissues contributing to its low expression compared to normal controls. Restoring HIC1 expression inhibited migration, invasion and promoted inducible apoptosis of NSCLC cells. Notably, HIC1 is a tumor suppressor through inhibiting the transcription of IL-6 by sequence-specific binding on its promoter. Restoring IL-6 expression could partially rescue these phenotypes induced by HIC1 in vitro and in vivo. Mechanistic analyses show that autocrine secretion of IL-6 induced by loss of HIC1 activated STAT3 through IL-6/JAK pathway and was associated with NSCLC progression. The HIC1/IL-6 axis may serve as a prognostic biomarker and provide an attractive therapeutic target for NSCLC.
刊物名称: ONCOTARGET
英文刊物名称: ONCOTARGET
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学科: Oncology; Cell Biology
英文学科: Oncology; Cell Biology
影响因子: 5.168
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论文类别: Article
英文论文类别: Article
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