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RASSF1A Suppresses the c-Jun-NH₂-Kinase Pathway and Inhibits Cell Cycle Progression

¹ Department of Internal Medicine and Brain Korea 21 Project for Biomedical Science; ² Genomic Research Center for Lung and Breast/Ovarian Cancers, Korea University Cancer Institute; and ³ Department of Internal Medicine and ⁴ Graduate School of Medicine, Korea University College of Medicine, Seoul, South Korea

Requests for reprints: Young Do Yoo, Graduate School of Medicine, Korea University College of Medicine, 136-705 Seoul, South Korea. Phone: 82-2-920-5762; Fax: 82-2-920-5762; E-mail: ydy{at}kumc.or.kr.

Some oncogenes, such as activated Ras, cause the malignant transformation of lung cells. c-Jun-NH₂-kinase (JNK) activation is essential for the oncogenic function of these cells. In this study, we show that RASSF1A inhibits the growth of lung cancer cells by blocking the JNK pathway. The exogenous expression of RASSF1A suppressed JNK phosphorylation, and cells stably transfected with RASSF1A showed reduced JNK and c-Jun phosphorylation and Cyclin D1 down-regulation. An in vitro kinase assay showed that the exogenous expression of RASSF1A inhibited JNK activity and that JNK activity suppression due to ectopically expressed RASSF1A was revived by RASSF1A siRNA treatment. Based on our data, we suggest that RASSF1A exerts a tumor-suppressing effect by blocking oncogene-mediated JNK activation in lung cells.

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