Panoply™ Human CEACAM1 Over-expressing Stable Cell Line

Vasculogenic mimicry (VM) promotes tumor migration, metastasis, and invasion in various cancers, but the relationship between VM and these phenotypes remains unclear. Here, researchers investigated carcinoembryonic antigen cell adhesion molecule 1 (CEACAM1) as a novel target for VM. They found that ectopic expression of CEACAM1 in HT1080 human fibrosarcoma cells inhibited the formation of VM-like networks. Furthermore, introduction of CEACAM1 into HT1080 cells also suppressed cell migration and proliferation. Conversely, knockout (KO) of CEACAM1 in SK-MEL-28 melanoma cells, which normally express high levels of CEACAM1, inhibited the formation of VM-like networks, whereas reintroduction of CEACAM1 abolished these networks. These results suggest that CEACAM1 differentially regulates the formation of VM-like networks across different cancer cell types and suggest that CEACAM1 is a novel therapeutic target for malignant cancers.

To determine whether CEACAM1 affects the formation of VM-like networks, the researchers established a CEACAM1-overexpressing HT1080 cell line (Figure 1A) and assessed its ability to form such networks on Matrigel. Overexpression of CEACAM1 significantly inhibited network formation on Matrigel (Figure 1B and C), indicating that CEACAM1 inhibits the formation of VM-like networks in HT1080 cells. Because CEACAM1 contributes to cancer cell migration, the researchers used a wound-healing assay to examine whether CEACAM1 expression regulates cancer cell migration in HT1080 cells. Overexpression of CEACAM1 reduced the migration rate of HT1080 cells compared to control cells (Figure 1D and E). Furthermore, CEACAM1 expression significantly reduced the proliferation rate of HT1080 cells compared to control cells (Figure 1F). These results indicate that CEACAM1 functions as a tumor suppressor gene in HT1080 cells.

Figure 1. Effect of CEACAM1 overexpression on VM-like network formation in HT1080 cells. (Hayashi S, et al., 2020)