CDX-2 overexpression

Our study demonstrates that anorectal NECs arise in HPV-dependent or independent pathways, with heterogeneous expression of other lineage markers and different molecular signatures. Expression of p53 and c-Myc proteins appear to be mutually exclusive regardless of HPV status, likely mediating alternative mechanisms of NEC carcinogenesis.

Upon treatment with lithium chloride (LiCl), the proliferation, migration, and invasion of CDX2-overexpressing MKN7 and TMK1 cells were enhanced. Our results indicate that Res inhibits the growth of MKN7 and TMK1 cells by increasing RUNX3 and CDX2 expression levels, with the potential involvement of the β-catenin/TCF-4 signaling pathway.

CDX2-induced up-regulation of miR-744 can significantly promote the migration and invasion of NSCLC cells, while overexpression CDX2 is sufficient to rescue the migration and invasion capacity of these cells following knockdown of miR-744. In summary, our results confirmed for the first time the regulatory mechanism of CDX2 on miR-744 transcription and provided a potential mechanism for CDX2 as an oncogene in lung cancer.

Our findings demonstrate that CDX2 expression was positively correlated with that of Reg IV in gastric cancer, and CDX2 promoted cell migration and invasion through upregulation of Reg IV expression in AGS and MKN-45 cells.