Open AccessTargeting MUC 1 and JNK by RNA interference and inhibitor inhibit the development of hepatocellular carcinoma
Author(s) -
Wang Juan,
Ni Weihua,
Hu Kebang,
Zhai Xiaoyu,
Xie Fei,
Jie Jing,
Zhang Nannan,
Jiang Lina,
Yuan Hongyan,
Tai Guixiang
Publication year - 2017
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.13144
Subject(s) - gene knockdown , gene silencing , rna interference , cancer research , oncogene , small interfering rna , carcinogenesis , small hairpin rna , transfection , hepatocellular carcinoma , chemistry , biology , medicine , rna , cell culture , cell , cancer , cell cycle , gene , biochemistry , genetics
Mucin 1 ( MUC 1), 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 ( RNA i) and JNK inhibitor SP 600125, which target MUC 1 and/or JNK , were used to treat HCC cells in vitro , and the results showed that both silencing the expression of MUC 1 and blocking the activity of JNK inhibited the proliferation of HCC cells. In addition, MUC 1‐stable‐knockdown and SP 600125 significantly inhibited the growth of tumors in the subcutaneous transplant tumor models that established in BALB /c nude mice rather than MUC 1 or JNK si RNA s transiently transfection. Furthermore, the results from immunohistochemical staining assays showed that the inhibitory effects of MUC 1 gene silencing and SP 600125 on the proliferation of HCC cells in vivo were through the JNK / TGF ‐β signaling pathway. These results indicate that MUC 1 and JNK are attractive targets for HCC therapy and may provide new therapeutic strategies for the treatment of HCC .