Objectives: Recently, embryonic microenvironment is being known for its non-permissive property for
tumor growth. However, the regulatory mechanism to maintain the balance between differentiation and tumorigenicity of
cancer cell in microenvironment is not well understood. Materials and Methods: qRT-PCR was performed to detect the levels of gene expression in HT29, LoVo and Caco-2
colorectal cancer cells, and Western blot was used to measure the
protein levels. Cell migration and apoptosis were measured by Transwell and flow cytometry assays.
Cancer cell markers were detected using immunohistochemical staining. In vivo
tumor formation assay was conducted by
subcutaneous injection of embryonic microenvironment-treated
cancer cells. Results:
Colorectal cancer cell lines were treated with human embryonic stem cell conditioned culture and then collected for in vivo
tumor formation assay and in vitro assays assessing the aggressive properties. We found exposure of
cancer cells in human ES cultures resulted in inhibition of growth, migration of
tumor cells. Moreover, we found that manipulation of Notch pathway in the ES cells microenvironment could influence the stemness of
tumor. We specifically discovered that some factor in the embryonic microenvironment could suppress Notch1 pathway in the
cancer cells, leading to a reduction in
tumorigenesis and invasiveness. Conclusions: This study may provide another evidence to understand the crosstalk between
tumor cells and embryonic environment and may offer new therapeutic strategies to inhibit
colorectal cancer progression.