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Vol. 56, Issue 6, 1271-1279, December 1999
Department of Microbiology and Immunology, Baylor College of
Medicine, Houston, Texas
N-(4-Hydroxyphenyl)retinamide (4-HPR), a retinoic acid
analog, induces apoptosis in several cell types. The mechanism by which 4-HPR initiates apoptosis remains poorly understood. We examined the
effects of 4-HPR on two prostate carcinoma cell lines, LNCaP (an
androgen-sensitive, p53+/+ cell line) and PC-3 (an
androgen-insensitive, p53
/ cell line). 4-HPR caused
sustained c-Jun N-terminal kinase (JNK) activation and apoptosis in
LNCaP cells but not in PC-3 cells at the dosages tested. Activation of
JNK by 4-HPR was independent of caspases because a pan-caspase
inhibitor failed to suppress JNK activation. Ultraviolet-C and
-radiation induced JNK activation in both LNCaP and PC-3 cells,
suggesting that the failure of PC-3 cells to respond to 4-HPR was due
to defects upstream of the JNK pathway. Furthermore,
-radiation-induced JNK activation was suppressed by an antioxidant,
but 4-HPR-induced JNK activation was not, indicating that these two
stimuli induced JNK activation through different mechanisms. Forced
expression of JNK1, but not a JNK1 mutant, caused apoptosis in both
LNCaP and PC-3 cells, suggesting that p53 is not required for
JNK-mediated apoptosis. 4-HPR-induced apoptosis in LNCaP cells was
suppressed by curcumin, which inhibits JNK activation. Expression of
dominant-negative mutants in the JNK pathway also inhibited
4-HPR-induced apoptosis in human embryonic kidney 293 cells.
Collectively, these results suggest that the JNK pathway mediates
4-HPR-induced apoptotic signaling.
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