2014年4月
TSPAN2 Is Involved in Cell Invasion and Motility during Lung Cancer Progression
CELL REPORTS
- 巻
- 7
- 号
- 2
- 開始ページ
- 527
- 終了ページ
- 538
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1016/j.celrep.2014.03.027
- 出版者・発行元
- CELL PRESS
In lung cancer progression, p53 mutations are more often observed in invasive tumors than in noninvasive tumors, suggesting that p53 is involved in tumor invasion and metastasis. To understand the nature of p53 function as a tumor suppressor, it is crucial to elucidate the detailed mechanism of the alteration in epithelial cells that follow oncogenic KRAS activation and p53 inactivation. Here, we report that KRAS activation induces epithelial-mesenchymal transition and that p53 inactivation is required for cell motility and invasiveness. Furthermore, TSPAN2, a transmembrane protein, is responsible for cell motility and invasiveness elicited by p53 inactivation. TSPAN2 is highly expressed in p53-mutated lung cancer cells, and high expression of TSPAN2 is associated with the poor prognosis of lung adenocarinomas. TSPAN2 knockdown suppresses metastasis to the lungs and liver, enabling prolonged survival. TSPAN2 enhances cell motility and invasiveness by assisting CD44 in scavenging intracellular reactive oxygen species.
- リンク情報
- ID情報
-
- DOI : 10.1016/j.celrep.2014.03.027
- ISSN : 2211-1247
- Web of Science ID : WOS:000335442300021