Senzaki H, Iwamoto S, Ogura E, Kiyozuka Y, Arita S, Kurebayashi J, Takada H, Hioki K, Tsubura A
Department of Pathology II, Kansai Medical University, Osaka, Japan.
Anticancer Res. 1998 May-Jun;18(3A):1621-7.
To evaluate the effects of dietary fats on breast cancer growth and metastasis, KPL-1 human breast carcinoma cells which have a propensity for axillary lymph node metastasis when inoculated into the thoracic mammary fat pad of female nude mice were examined. The mice were fed one of three semipurified diets containing 9.5% eicosapentaenoic acid plus 0.5% linoleic acid (EPA diet), 10% linoleic acid (LA diet), or 9.5% palmitic acid plus 0.5% linoleic acid (PA diet), or commercial laboratory chow containing 8.5% fat of which 4.1% was LA, 1.1% was PA, 0.06% was EPA, and 3.24% was other (Standard diet) starting 19 days before tumor cell inoculation and continuing until the end of the experiment (43 days after tumor cell inoculation). The tumor growth was faster and at a higher incidence in the mice fed the LA diet, and much slower and at a lower incidence in the EPA diet group compared with the mice fed the PA or Standard diet; the two separate experiment demonstrated identical results. The differences in tumor weight between the LA and PA groups and between the PA and EPA groups were significant (P < 0.05, respectively) at the termination of the experiment; the differences were due to different tumor cell proliferation rates. In an in vitro MTT assay, fatty acids showed direct stimulatory or inhibitory effects on the KPL-1 cells. Lymph node metastasis was seen in the LA and Standard diet groups, whereas it was not seen in the PA or EPA groups. The body weights were significantly lighter in the LA and EPA groups compared with the PA and Standard diet groups (P < 0.05, respectively). The results indicate that the EPA diet produced a reduction in tumor cell growth and metastasis whereas the LA diet had an enhancing effect on these parameters; dietary fatty acids may thus have a direct role in the growth and metastasis of human breast carcinoma independent of their systemic effects.
为了评估膳食脂肪对乳腺癌生长和转移的影响,研究人员对KPL - 1人乳腺癌细胞进行了检测。当将这些细胞接种到雌性裸鼠的胸部乳腺脂肪垫中时,它们有腋窝淋巴结转移的倾向。在肿瘤细胞接种前19天开始,给小鼠喂食三种半纯化饮食之一,分别含9.5%二十碳五烯酸加0.5%亚油酸(EPA饮食)、10%亚油酸(LA饮食)或9.5%棕榈酸加0.5%亚油酸(PA饮食),或者喂食含8.5%脂肪的商业实验室饲料(标准饮食),其中4.1%是亚油酸,1.1%是棕榈酸,0.06%是二十碳五烯酸,3.24%是其他脂肪酸,持续到实验结束(肿瘤细胞接种后43天)。与喂食PA或标准饮食的小鼠相比,喂食LA饮食的小鼠肿瘤生长更快且发生率更高,而EPA饮食组的肿瘤生长慢得多且发生率更低;两项独立实验结果相同。在实验结束时,LA组和PA组之间以及PA组和EPA组之间的肿瘤重量差异显著(分别为P < 0.05);这些差异是由于不同的肿瘤细胞增殖率所致。在体外MTT试验中,脂肪酸对KPL - 1细胞表现出直接的刺激或抑制作用。在LA组和标准饮食组中观察到淋巴结转移,而在PA组或EPA组中未观察到。与PA组和标准饮食组相比,LA组和EPA组的体重明显更轻(分别为P < 0.05)。结果表明,EPA饮食可减少肿瘤细胞生长和转移,而LA饮食对这些参数有增强作用;因此,膳食脂肪酸可能在人乳腺癌的生长和转移中具有直接作用,而与其全身效应无关。