Kruppel-like factor 2 inhibits hepatocarcinogenesis through negative regulation of the Hedgehog pathway

被引：30
|
作者：
Lin, JinBo [1 ]
Tan, Huifang [2 ]
Nie, Yingjie [3 ]
Wu, Dongwen [4 ]
Zheng, Weiji [1 ]
Lin, Wensong [1 ]
Zhu, Zheng [1 ]
Yang, Bing [1 ]
Chen, Xiaoliang [5 ]
Chen, Tao [2 ,3 ]
机构：
[1] Zunyi Med Univ, Affiliated Longgang Hosp, Longgang Cent Hosp Shenzhen, Shenzhen, Peoples R China
[2] Guangzhou Med Univ, Affiliated Hosp 1, Guangzhou, Guangdong, Peoples R China
[3] Guizhou Prov Peoples Hosp, Clin Res Lab Ctr, Guiyang, Guizhou, Peoples R China
[4] Cent South Univ, Xiangya Hosp 3, Changsha, Hunan, Peoples R China
[5] Shenzhen Guangming Dist Ctr Dis Prevent & Control, Shenzhen, Peoples R China
来源：
CANCER SCIENCE | 2019年 / 110卷 / 04期
关键词：
HDAC1; Hedgehog signaling; hepatocellular carcinoma; intrahepatic metastasis; Kruppel-like factor 2; NONCODING RNA ANRIL; CELL LUNG-CANCER; HEPATOCELLULAR-CARCINOMA; DOWN-REGULATION; PROLIFERATION; MIGRATION; INVASION; GROWTH; KLF2; TRANSCRIPTION;
D O I：
10.1111/cas.13961
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. The most important reason for the occurrence of HCC is hepatitis C or B infection. Moreover, genetic factors play an important role in the tumorigenesis of HCC. Here, we demonstrated that Kruppel-like factor 2 (KLF2) expression was downregulated in HCC samples compared with adjacent tissues. Additionally, KLF2 was shown to inhibit the growth, migration and colony-formation ability of liver cancer cells. Further mechanistic studies revealed that KLF2 can compete with Gli1 for interaction with HDAC1 and restrains Hedgehog signal activation. Together, our results suggest that KLF2 has potential as a diagnostic biomarker and therapeutic target for the treatment of HCC.
引用
收藏
页码：1220 / 1231
页数：12
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