Emerging clinical significance of claudin-7 in colorectal cancer: a review

Abstract

Tight junctions (TJs) play an important role in maintaining cell polarity and regulating cell permeability. In recent years, many studies have shown that TJ proteins, especially claudin-7, are closely related to inflammation and the development of various malignant tumors. Claudin-7 plays a significant role in maintaining the physiological functions and pathological conditions of the TJ barrier. The dysregulation of claudin-7 plays a tumor suppressor role or conversely has carcinogenic effects in different target tissues or cells, but the exact underlying mechanism is still unclear. 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. The construction of Cldn7^-/- mice and conventional claudin-7 knockout mouse models has helped determine the mechanisms by which claudin-7 promotes tumorigenesis. Elucidation of the expression and subcellular localization of claudin-7 under pathological conditions will help develop claudin-7 as a useful biomarker for detecting and diagnosing cancer, and thus may help combat the occurrence, development, and invasion of cancers.

Keywords: claudin-7; colorectal cancer; invasion; metastasis; tight junctions; tumors.

Figure 1

The junctional complex in epithelial and endothelial cells. Notes: Tight junctions (blue) and adherens junctions (yellow) are apically located in polarized epithelial cells and endothelial cells. Claudin-7 (red) is not only localized at apical intestinal epithelial cells but also has a strong basolateral and basement membrane distribution in the intestines. Dysregulation of claudin-7 expression and subcellular localization can promote inflammation, EMT, and cancer progression. Abbreviation: EMT, epithelial–mesenchymal transition.