Kim Seo Young, Kim Jong-Eun, Lee Ki Won, Lee Hyong Joo
Major in Biomodulation, Department of Agricultural Biotechnology, Seoul National University, Seoul, Korea.
Ann N Y Acad Sci. 2009 Aug;1171:270-5. doi: 10.1111/j.1749-6632.2009.04721.x.
We investigated the antiproliferative effects of the cytoplasmic fraction of Lactococcus lactis ssp. lactis (L.lac CF) on the SNU-1 human stomach cancer cell line. The proliferation of SNU-1 cells was inhibited by treatment with L.lac CF in a time- and dose-dependent manner. L.lac CF caused G0/G1 cell cycle arrest, which was associated with an increase in p53 and p21 expression, the reduction of cyclin D1 expression, and retinoblastoma protein phosphorylation. L.lac CF induced apoptosis in SNU-1 cells, as demonstrated by increased nucleus condensation and a sub-G1 peak. Caspase-3 activation, the induction of p53, and the downregulation of Bcl-2 were also observed in L.lac CF-treated cells. Thus, the inhibitory effect of L.lac CF on SNU-1 cell growth is mainly attributable to the induction of G0/G1 cell cycle arrest and apoptosis.
我们研究了乳酸乳球菌亚种乳酸乳球菌（L.lac CF）的细胞质组分对SNU-1人胃癌细胞系的抗增殖作用。用L.lac CF处理可抑制SNU-1细胞的增殖，且呈时间和剂量依赖性。L.lac CF导致G0/G1期细胞周期停滞，这与p53和p21表达增加、细胞周期蛋白D1表达降低以及视网膜母细胞瘤蛋白磷酸化有关。L.lac CF诱导SNU-1细胞凋亡，表现为细胞核浓缩增加和亚G1峰。在L.lac CF处理的细胞中还观察到半胱天冬酶-3激活、p53诱导和Bcl-2下调。因此，L.lac CF对SNU-1细胞生长的抑制作用主要归因于诱导G0/G1期细胞周期停滞和凋亡。
