Qiao L, Shiff S J, Rigas B
Department of Medicine, Cornell University Medical College, New York, NY 10021, USA.
Cancer Lett. 1997 May 19;115(2):229-34. doi: 10.1016/s0304-3835(97)04740-x.
We evaluated the effect of sulindac sulfide (SS), which reduces cell number and induces apoptosis in cultured colon cancer cells (CCCs), on expression of the proliferation markers PCNA and Ki-67 in HT-29 and HCT-15 CCCs; only the former express cyclooxygenases. DNA content and PCNA/Ki-67 expression were analyzed by bivariate flow cytometry. SS inhibited cell proliferation, determined by the reduced expression of PCNA and Ki-67, roughly by half at 72 h, and induced apoptosis (accounting for about two-thirds and one-third of the reduction in cell number, respectively). A similar effect of SS occurred in HT-29 and HCT-15 CCCs, and also in non-colonic cells, indicating that this rather general effect of SS on cultured cells is not dependent on inhibition of prostaglandin synthesis.
我们评估了舒林酸硫化物(SS)对HT - 29和HCT - 15结肠癌细胞(CCC)中增殖标志物PCNA和Ki - 67表达的影响,SS可减少培养的结肠癌细胞数量并诱导其凋亡;只有前者表达环氧化酶。通过双变量流式细胞术分析DNA含量以及PCNA/Ki - 67表达。SS抑制细胞增殖,这可通过PCNA和Ki - 67表达降低来确定,在72小时时大约抑制一半,并且诱导凋亡(分别占细胞数量减少的约三分之二和三分之一)。SS在HT - 29和HCT - 15 CCCs以及非结肠细胞中产生类似作用,表明SS对培养细胞的这种相当普遍的作用不依赖于前列腺素合成的抑制。