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TAp73 inhibits cell invasion and migration by directly activating KAI1 expression in colorectal carcinoma
  • 작성일2019-05-09
  • 최종수정일2019-05-09
  • 담당부서연구기획과
  • 연락처043-719-8033
  • 799
Cancer Letters, 2018, 415, 106─116, DOI: https://doi.org/10.1016/j.canlet.2017.12.002

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

Woo-Kyun Bae, Mi-Ra Park; Eun-Gene Sun; Ji-Hee Lee; Keunsoo Kang; Kyung-Hyun Ryu; Hyun-Jeong Shim; Jun-Eul Hwang; Sang-Hee Cho; Ik-Joo Chung

Abstract

    p73 is a member of the p53 family of tranion 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 tranional 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 tranion of KAI1.



  • 본 연구는 질병관리본부 연구개발과제(과제번호 2018-보건의료생물자원종합관리) 연구비를 지원받아 수행되었습니다.
  • This research was supported by a fund(code 2018-보건의료생물자원종합관리) by Research of Korea Centers for Disease Control and Prevention.


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