期刊
MOLECULAR CARCINOGENESIS
卷 53, 期 -, 页码 E161-E168出版社
WILEY-BLACKWELL
DOI: 10.1002/mc.22083
关键词
ZNF143; migration; invasion; ZEB1; E-cadherin
资金
- National Cancer Center [1110022]
- National Research Foundation of Korea [22A20130000078] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
To investigate the role of zinc-finger protein 143 in cancer cells, we stably introduced ZNF143 expression knockdown by infecting colon cancer cells with short hairpin (sh) RNA-lentiviral particles against ZNF143 (HCT116 sh-ZNF143). Compared to sh-control cells, HCT116 sh-ZNF143 cells showed faster wound healing, increased migration through Transwell chambers, and increased invasion through Matrigel in Transwell chambers. ZNF143 knockdown increased transcriptional expression of ZEB1. Additionally, ZNF143 regulated E-cadherin transcriptional expression. Small interfering-RNA-mediated silencing of ZEB1 expression affected motility in HCT116 sh-ZNF143 cells. These data suggest that ZNF143 is involved in cellular motility through a ZEB1-E-cadherin-linked pathway in colon cancer cells. (c) 2013 Wiley Periodicals, Inc.
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