Wang T T, Phang J M
Laboratory of Nutritional and Molecular Regulation, NCI-Frederick Cancer Research and Development Center, NIH, MD 21702-1201, USA.
Cancer Lett. 1996 Oct 1;107(1):65-71. doi: 10.1016/0304-3835(96)04344-3.
The synthetic retinoid N-(4-hydroxyphenyl)retinamide (4-HPR) has been used in breast cancer prevention and treatment. However, the molecular mechanisms mediating the effects of 4-HPR remain elusive. In the present study, we examined the effects of 4-HPR on components of apoptosis pathway (i.e Bcl-2 and Bax) and apoptotic death in both estrogen receptor-positive and estrogen receptor-negative cell lines. We found that: (1) 4-HPR treatment resulted in decreased Bcl-2 mRNA but not Bax mRNA levels; (2) the effect of 4-HPR on Bcl-2 mRNA level was different from other retinoids; (3) 4-HPR treatment induced apoptosis in both estrogen receptor-positive and -negative cells. Hence, the breast cancer chemopreventive properties of 4-HPR may involve modulation of apoptosis pathways.
合成维甲酸N-(4-羟基苯基)视黄酰胺(4-HPR)已用于乳腺癌的预防和治疗。然而，介导4-HPR作用的分子机制仍不清楚。在本研究中，我们检测了4-HPR对雌激素受体阳性和雌激素受体阴性细胞系中凋亡途径成分(即Bcl-2和Bax)及凋亡死亡的影响。我们发现：(1) 4-HPR处理导致Bcl-2 mRNA水平降低，但Bax mRNA水平未降低；(2) 4-HPR对Bcl-2 mRNA水平的影响与其他维甲酸不同；(3) 4-HPR处理诱导雌激素受体阳性和阴性细胞凋亡。因此，4-HPR的乳腺癌化学预防特性可能涉及凋亡途径的调节。
