Open AccessKrüppel‐like factor 2 inhibits hepatocarcinogenesis through negative regulation of the Hedgehog pathway
Author(s) -
Lin JinBo,
Tan Huifang,
Nie Yingjie,
Wu Dongwen,
Zheng Weiji,
Lin Wensong,
Zhu Zheng,
Yang Bing,
Chen Xiaoliang,
Chen Tao
Publication year - 2019
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.13961
Subject(s) - klf2 , krüppel , hepatocellular carcinoma , hedgehog , cancer research , carcinogenesis , biomarker , gli1 , hedgehog signaling pathway , biology , cancer , hdac1 , liver cancer , transcription factor , signal transduction , medicine , genetics , dna , histone deacetylase , gene , histone
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 Krüppel‐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.