Claudin-7 may inhibit the proliferation and migration of tumor cells by interacting with integrinβ1, subsequently participating in the development of colorectal cancer.
Claudin-7, one of the important components of cellular tight junctions, is currently considered to be expressed abnormally in colorectal inflammation and colorectal cancer.
In this review, we will summarize the expression pattern of claudin-7 in tumors, focusing on the expression and regulation of claudin-7 in colorectal cancer and discussing the correlation between claudin-7 and invasion, metastasis and epithelial-mesenchymal transition (EMT) in colorectal cancer.
As a potential tumor suppressor gene, Claudin-7 (Cldn7), which is a component of tight junctions, may play an important role in colorectal cancer occurrence and development.
Thus, our data suggest that miR-155 plays an important role in promoting CRC cell migration and invasion, at least in part through the regulation of claudin-1 expression and controlling metastasis in CRC.
The expression of CL-1 at the mRNA and protein levels was analyzed in 41 cases and was found to increase in the CRC tissue in comparison to that in the normal tissue specimens.
These findings suggest that the CLDN7 gene silencing by promoter hypermethylation and the resultant reduction of CLDN7 expression may play an important role in the progression of CRCs.
In the present study, we report an inverse relationship between Smad4 and claudin-1 expression in human colorectal carcinoma tumor samples and in human colon cancer cell lines.