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Cancer Lett. 2002 May 8;179(1):51-8.

Methionine restriction induces apoptosis of prostate cancer cells via the c-Jun N-terminal kinase-mediated signaling pathway.

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Department of Medicine, Baylor College of Medicine, and Houston VA Medical Center, Medical Service (111H), 2002 Holcombe Boulevard, Houston, TX 77030, USA.


Tumors are relatively more sensitive to methionine restriction than corresponding normal tissues, a phenomenon known as methionine auxotrophy. The current studies were undertaken to elucidate the molecular mechanisms for methionine auxotrophy of prostate cancer cells. We found that the activity of c-Jun N-terminal kinase 1 (JNK1) increased dramatically in response to methionine restriction. Over expression of wild type JNK1 by transient transfection enhanced apoptosis in response to methionine restriction, whereas over expression of a kinase inactive mutant of JNK1 protected PC-3 human prostate cancer cells from apoptosis. We conclude that JNK1 plays a critical role in signaling cancer cells to undergo apoptosis in response to methionine restriction.

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