Phosphatidylinositol 3-kinase mediates bronchioalveolar stem cell expansion in mouse models of oncogenic K-ras-induced lung cancer.
Phosphatidylinositol 3-kinase mediates bronchioalveolar stem cell expansion in mouse models of oncogenic K-ras-induced lung cancer.
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磷脂酰肌醇3-激酶在致癌性K-RAS诱导的肺癌的小鼠模型中介导支气管肺泡干细胞的扩张。
DOI：
10.1371/journal.pone.0002220
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发表时间：
2008-05-21
期刊：
影响因子：
3.7
通讯作者：
Kurie, Jonathan M.
中科院分区：
文献类型：
--
作者：
Yang, Yanan;Iwanaga, Kentaro;Raso, Maria Gabriela;Wislez, Marie;Hanna, Amy E.;Wieder, Eric D.;Molldrem, Jeffrey J.;Wistuba, Ignacio I.;Powis, Garth;Demayo, Francesco J.;Kim, Carla F.;Kurie, Jonathan M.
Non-small cell lung cancer (NSCLC) is the most common cause of cancer-related death in Western countries. Developing more effective NSCLC therapeutics will require the elucidation of the genetic and biochemical bases for this disease. Bronchioalveolar stem cells (BASCs) are a putative cancer stem cell population in mouse models of oncogenic K-ras-induced lung adenocarcinoma, an histologic subtype of NSCLC. The signals activated by oncogenic K-ras that mediate BASC expansion have not been fully defined. We used genetic and pharmacologic approaches to modulate the activity of phosphatidylinositol 3-kinase (PI3K), a key mediator of oncogenic K-ras, in two genetic mouse models of lung adenocarcinoma. Oncogenic K-ras-induced BASC accumulation and tumor growth were blocked by treatment with a small molecule PI3K inhibitor and enhanced by inactivation of phosphatase and tensin homologue deleted from chromosome 10, a negative regulator of PI3K. We conclude that PI3K is a critical regulator of BASC expansion, supporting treatment strategies to target PI3K in NSCLC patients.
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