Title

Role of JNK in tumor development

UMMS Affiliation

Howard Hughes Medical Institute and Program in Molecular Medicine

Date

5-8-2003

Document Type

Article

Subjects

Animals; Apoptosis; Cell Transformation, Neoplastic; Enzyme Inhibitors; Eukaryotic Cells; Humans; JNK Mitogen-Activated Protein Kinases; Mitogen-Activated Protein Kinases; Neoplasms; Signal Transduction; Tumor Suppressor Proteins; ras Proteins

Disciplines

Life Sciences | Medicine and Health Sciences

Abstract

The c-Jun NH2-terminal kinase (JNK) is implicated in oncogenic transformation. However, studies of the effect of Jnk gene disruption on Ras-induced transformation of murine fibroblasts indicate that JNK may act as a suppressor of Ras transformation and that the JNK signaling pathway contributes to the apoptotic elimination of transformed cells in vivo. The conclusion that JNK can act as a tumor suppressor is consistent with the presence of loss-of-function mutations in JNK pathway components (Jnk3 and Mkk4) in human tumors. Nevertheless, JNK can also contribute to the proliferation and survival responses of some tumors. A key question that remains unresolved concerns the genetic and mechanistic basis for these different roles of JNK in tumors. Indeed, an understanding of this question will be required for the rational use of small molecule inhibitors of JNK for tumor therapy.

Rights and Permissions

Citation: Cell Cycle. 2003 May-Jun;2(3):199-201.

Related Resources

Link to article in PubMed

Journal Title

Cell cycle (Georgetown, Tex.)

PubMed ID

12734425