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通过RNA干扰和抑制剂靶向MUC1和JNK可抑制肝细胞癌的发展。

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

作者信息

Wang Juan, Ni Wei-Hua, Hu Ke-Bang, Zhai Xiao-Yu, Xie Fei, Jie Jing, Zhang Nan-Nan, Jiang Li-Na, Yuan Hong-Yan, Tai Gui-Xiang

机构信息

Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun, China.

Department of Urology, The First Hospital of Jilin University, Changchun, China.

出版信息

Cancer Sci. 2017 Mar;108(3):504-511. doi: 10.1111/cas.13144.

DOI:10.1111/cas.13144
PMID:28012230
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5378288/
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.

摘要

黏蛋白1（MUC1）作为一种癌基因，在肝细胞癌（HCC）细胞中过表达，并通过JNK/TGF-β信号通路促进HCC的进展和肿瘤发生。在本研究中，使用靶向MUC1和/或JNK的RNA干扰（RNAi）和JNK抑制剂SP600125在体外处理HCC细胞，结果表明，沉默MUC1的表达和阻断JNK的活性均抑制了HCC细胞的增殖。此外，MUC1稳定敲低和SP600125显著抑制了在BALB/c裸鼠中建立的皮下移植瘤模型中的肿瘤生长，而不是MUC1或JNK siRNAs瞬时转染。此外，免疫组织化学染色分析结果表明，MUC1基因沉默和SP600125对体内HCC细胞增殖的抑制作用是通过JNK/TGF-β信号通路实现的。这些结果表明，MUC1和JNK是HCC治疗的有吸引力的靶点，可能为HCC的治疗提供新的治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3c7/5378288/342c164d51d9/CAS-108-504-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3c7/5378288/59610ee99b2c/CAS-108-504-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3c7/5378288/6321c7b07aba/CAS-108-504-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3c7/5378288/342c164d51d9/CAS-108-504-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3c7/5378288/00b0e034b03a/CAS-108-504-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3c7/5378288/37902afa0e69/CAS-108-504-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3c7/5378288/b8b8b2d4ca02/CAS-108-504-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3c7/5378288/59610ee99b2c/CAS-108-504-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3c7/5378288/342c164d51d9/CAS-108-504-g006.jpg

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黏蛋白1的表达受hsa_circ_0055054/微小RNA-122-5p调控，并促进肝细胞癌的发展。
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