期刊
JOURNAL OF CANCER
卷 10, 期 6, 页码 1375-1384出版社
IVYSPRING INT PUBL
DOI: 10.7150/jca.29932
关键词
SUZ12; Hepatocellular carcinoma; Migration; Invasion; ERK1/2
类别
资金
- Science and Technology Program of Guangzhou [201707010470]
- National Natural Science Foundation of China [81372634, 81600350]
- Guangdong Natural Science Funds for Distinguished Young Scholar [S2013050014121]
- Guangdong Province Office of Education [2015KTSCX117]
The suppressor of zest 12 (SUZ12), an essential subunit of the transcription polycomb repressive complex 2 (PRC2), has been found to be involved in HBV X-induced oncogenic transformation in hepatocellular carcinoma (HCC). However, the specific function of SUZ12 has not yet been determined in the pathogenesis of migration and invasion of HBV-associated HCC. Here, our results showed that SUZ12 was significantly down-regulated in HBV-related HCC tissues compared with adjacent non-tumor tissues by immunohistochemical and Western blot assays. The 5-years survival rate was worse in patients with low expression level of SUZ12. SUZ12 silencing increased the migration and invasion of HCC cells, and its overexpression impaired HCC cells migration and invasion. Knockdown of SUZ12 activated ERKI/2 pathway and increased MMP9 (matrix metallopeptidase 9) and MMP2 (matrix metallopeptidase 2) expression, whereas SUZ12 overexpression had opposite effects. Specific ERKI/2 inhibitor (SCH772984) significantly decreased HCC cells migration and invasion caused by SUZ12 shRNA. Thus, the liver cancer-down-regulated SUZ12 accelerated the invasion and metastasis of HCC cells. These effects might be associated with deregulation of SUZ12 activating ERKI/2, MMP2 and MMP9 in HCC cells.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据