Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8292804 | Biochemical and Biophysical Research Communications | 2018 | 8 Pages |
Abstract
Cell division cycle associated 3 (CDCA3) is required for mitotic entry, and mediates the degradation of the inhibitory kinase Wee1. New evidence suggests CDCA3 plays a role in tumor promotion. However, little is known about the relevance of CDCA3 in colorectal cancer(CRC), especially in the regulation of NF-κB activity. In this study, we found that colorectal tumors significantly expressed more CDCA3 than non-cancer tissues. In addition, CDCA3 promoted CRC cell proliferation in vitro. Furthermore, downregulation of CDCA3 not only induced cell cycle arrest but also facilitated apoptosis. Mechanistically, CDCA3 activates the NF-κB signaling pathway by interacting with TRAF2 in CRC. Together, these results define a tumor-supportive role for CDCA3, which may also provide a new promising strategy for treating CRC.
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Authors
Wei Zhang, Yanxia Lu, Xiaomin Li, Jianming Zhang, Lin Zheng, Wenjuan Zhang, Chun Lin, Weihao Lin, Xuenong Li,