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Targeting MUC1 and JNK by RNA interference and inhibitor inhibit the development of hepatocellular carcinoma.

Authors
  • Wang, Juan1
  • Ni, Wei-Hua1
  • Hu, Ke-Bang2
  • Zhai, Xiao-Yu1
  • Xie, Fei1
  • Jie, Jing1
  • Zhang, Nan-Nan1
  • Jiang, Li-Na1
  • Yuan, Hong-Yan1
  • Tai, Gui-Xiang1
  • 1 Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun, China. , (China)
  • 2 Department of Urology, The First Hospital of Jilin University, Changchun, China. , (China)
Type
Published Article
Journal
Cancer science
Publication Date
Mar 01, 2017
Volume
108
Issue
3
Pages
504–511
Identifiers
DOI: 10.1111/cas.13144
PMID: 28012230
Source
Medline
Keywords
License
Unknown

Abstract

Mucin 1 (MUC1), as an oncogene, is overexpressed in hepatocellular carcinoma (HCC) cells and promotes the progression and tumorigenesis of HCC through JNK/TGF-β signaling pathway. In the present study, RNA interference (RNAi) and JNK inhibitor SP600125, which target MUC1 and/or JNK, were used to treat HCC cells in vitro, and the results showed that both silencing the expression of MUC1 and blocking the activity of JNK inhibited the proliferation of HCC cells. In addition, MUC1-stable-knockdown and SP600125 significantly inhibited the growth of tumors in the subcutaneous transplant tumor models that established in BALB/c nude mice rather than MUC1 or JNK siRNAs transiently transfection. Furthermore, the results from immunohistochemical staining assays showed that the inhibitory effects of MUC1 gene silencing and SP600125 on the proliferation of HCC cells in vivo were through the JNK/TGF-β signaling pathway. These results indicate that MUC1 and JNK are attractive targets for HCC therapy and may provide new therapeutic strategies for the treatment of HCC.

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