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Objectives A small subpopulation of colorectal cancer stem cells (CSCs) possess the ability to self-renew and the capacity to initiate the original tumor. EpCAMhigh/CD44+ cells are regarded as CSCs in colorectal cancer. The present study was undertaken to investigate the significance of EpCAM in the in vitro proliferation ability and oxaliplatin chemoresistance of EpCAMhigh/CD44+ colorectal CSCs. Methods We applied fluorescence-activated cell sorting (FACS) to separate the EpCAMhigh/CD44+ subset from human colorectal cancer cell line HCT116. We also used siRNA targeting EpCAM to create EpCAM−/CD44+ subpopulation. Then we compared EpCAMhigh/CD44+ cells and EpCAM−/CD44+ cells for proliferation ability and the chemoresistance to oxaliplatin by CCK8 assay. Results The EpCAMhigh/CD44+ subset comprises almost 6.25 ± 0.09% in cell line HCT116, and the EpCAM−/CD44+ cells displayed a significantly lower proliferation ability and weaker oxaliplatin chemoresistance than the EpCAMhigh/CD44+ cells. Conclusions EpCAM is critical for tumor proliferation and oxaliplatin chemoresistance in EpCAMhigh/CD44+ colorectal CSCs.

Aims: The present study investigated the exact proportion, the extent of in vitro proliferation potential, and oxaliplatin chemoresistance of EpCAMhigh/CD44+ cancer stem cells in colorectal cancer. Its underlying mechanism was also explored. Background: Colorectal cancer stem cells (CSC) play crucial roles in tumorigenicity and chemoresistance. Multiple studies have shown that JAK/STAT, NOTCH, and Wnt/-catenin pathways, associated with tumour recurrence and metastasis, contribute to the proliferation and maintenance of CSCs. CSCs become resistant to chemo-radiotherapies by improving DNA damage repair, changing cell cycle checkpoints, and scavenging reactive oxygen species, resulting in a bad patient prognosis. Objective: This work was carried out to determine the precise fraction, the degree of in vitro proliferation capability, and the level of oxaliplatin chemoresistance exhibited by EpCAMhigh/CD44+ cancer stem cells in colorectal cancer. The research was also done to investigate its underlying process. Methods: Fluorescence-activated cell sorting (FACS) was applied to isolate the EpCAMhigh/CD44+ populations from three human colorectal cancer cell lines (HCT116, HT29, and LoVo), and we quantified the average proportion of the EpCAMhigh/CD44+ cells in every cell lines. The comparison of their proliferation ability and the chemoresistance to oxaliplatin with the parental cells was estimated by CCK8 assay. The activated signaling pathway was tested by Western Blotting. result: EpCAMhigh/CD44+ subpopulation comprise about 4.98±1.24% of the total human colorectal cancer cell lines, and the EpCAMhigh/CD44+ cells exhibited a highly better proliferation ability and stronger oxaliplatin chemoresistance than the parental cells. Wnt/β-catenin signaling pathway is activated in EpCAMhigh/CD44+ HCT116 cells. Results: EpCAMhigh/CD44+ subpopulation comprises about 4.98±1.24% of the total human colorectal cancer cell lines, and the EpCAMhigh/CD44+ cells exhibited a highly better proliferation ability and stronger oxaliplatin chemoresistance than the parental cells. The wnt/β-catenin signaling pathway is activated in EpCAMhigh/CD44+ HCT116 cells conclusion: Activation of Wnt/β-Catenin signaling in EpCAMhigh/CD44+ cells endow colorectal cancer with tumor proliferation and oxaliplatin chemoresistance. Conclusion: Activation of Wnt/β-Catenin signaling in EpCAMhigh/CD44+ cells endow colorectal cancer with tumor proliferation and oxaliplatin chemoresistance.

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