In this study,CD133+ subpopulations were isolated from 41 primary colorectal cancer tissues,the proliferation and cell cycle distribution of the cells were examined without in vitro expansion,and then compared to those of cell lines.The detection of CD133 in colorectal cancer tissues,isolation of CD133+ and CD133-epithelial subpopulations,Ki-67/DNA multiparameter assay and cell volume analysis were flow cytometrically conducted.The results showed that Ki-67 expression was correlated with CD133 level in primary cancer tissues,while cell cycle G 2 /M phase distribution or clinicopathological characteristics was not.In addition,the CD133+ cells showed larger cell volume and higher Ki-67 expression as compared with CD133-cells.But there was no statistically significant difference in G 2 /M phase distribution between the two subpopulations.Our results demonstrated that the CD133+ subpopulation in colorectal cancer tissue contained more actively cycling and proliferating cells,which was not correlated to clinicopathological factors but might contribute to tumor progression and poor clinical outcome.
The forkhead family members of transcription factors （FoxOs） are expected to be potential cancer-related drug targets and thus are being extremely studied recently. In the present study, FoxO3a, one major member of this family, was identified to be down-regulated in colorectal cancer through mi- cro-array analysis, which was confirmed by RT-PCR and Western blot in 28 patients. Moreover, immu- nohistochemistry （IHC） showed that the expression levels of FoxO3a were remarkably reduced in 99 cases of primary colorectal cancer, liver metastasis, and even in metaplastic colorectal tissue. IHC also revealed an exclusion of FoxO3a from the nucleus of most cells of tumor-associated tissues. Silencing FoxO3a by siRNA led to elevation of G2-M phase cells. We conclude that the downregulation of FoxO3a may greatly contribute to tumor development, and thus FoxO3a may represent a novel thera- peutic target in colorectal cancer.
