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TAp73 inhibits cell invasion and migration by directly activating KAI1 expression in colorectal carcinoma

Authors
Bae, Woo-KyunHong, Chang-SooPark, Mi-RaSun, Eun-GeneLee, Ji-HeeKang, KeunsooRyu, Kyung-HyunShim, Hyun-JeongHwang, Jun-EulCho, Sang-HeeChung, Ik-Joo
Issue Date
Feb-2018
Publisher
ELSEVIER IRELAND LTD
Keywords
p73; KAI1; Invasion; Migration; Colorectal cancer
Citation
CANCER LETTERS, v.415, pp 106 - 116
Pages
11
Journal Title
CANCER LETTERS
Volume
415
Start Page
106
End Page
116
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/4692
DOI
10.1016/j.canlet.2017.12.002
ISSN
0304-3835
1872-7980
Abstract
p73 is a member of the p53 family of transcription factors and, like p53, plays a role as a tumor suppressor. p73 is involved in development, proliferation, apoptosis and metastasis. However, the precise molecular mechanisms underlying its function in inhibiting metastasis remain largely unknown. Here, we show that induction of TAp73 decreased invasion and migration activity of colorectal cancer cells, whereas knockdown of TAp73 led to increased invasion and migration activity. KAI1 was identified as a transcriptional target of TAp73 and its expression is indispensable for TAp73-mediated inhibition of cell invasion and migration. Furthermore, induction of TAp73 in colorectal cancer cells elevated KAI1 expression and decreased the frequency of hepatic metastasis in vivo. Whereas, the decreased invasion and migration activities caused by TAp73 induction were abrogated by knockdown of KAI1. Interestingly, TAp73 and KAI1 are overexpressed in primary colorectal cancers and a significant correlation between TAp73 and KAI1 expression was detected, but their expressions were significantly down-regulated in metastatic cancers. Taken together, our results support a novel role for TAp73 in controlling colorectal cancer cell invasion, migration and metastasis by regulating transcription of KAI1. (C) 2017 Elsevier B.V. All rights reserved.
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