Tight junction claudin-7 protein modulates multiple processes of cancer progression in human lung cancer cells

Abstract

Carcinogenesis usually consists of cancer initiation, promotion, and progression. Several tight junction claudin proteins have been identified as tumor suppressors or activators during cancer development. As apical proteins, tight junction claudins seal the apical sides of neighboring epithelial cells in regulating the transport of ions and fluids from the extracellular environment. However, claudin-7, which is believed to direct cell-matrix adhesion, has been found at the basal side of several human organs, including the lung. It has also been clinically reported that the low survival rate of lung cancer patients is closely associated with their low claudin-7 expression. The molecular mechanism of claudin-7 that regulates lung cancer progression is not clearly understood. In order to understand how claudin-7 is involved in lung carcinogenesis, this dissertation presents the molecular and cellular changes in human lung cancer cells upon the suppression of claudin-7 expression to study how claudin-7 modulates lung cancer cell progression, including cell proliferation, migration, and invasion, cell-matrix attachment, and cell metabolism.