Tns1, short for tensin1, is a member of the tensin family, which are cellular-adhesion constituents. Tns1 engages in multiple biological processes such as cell adhesion, polarization, migration, invasion, proliferation, apoptosis, and mechano-transduction by interacting with various partner proteins. Abnormal Tns1 expression in vivo is associated with the development of various diseases, especially tumors. Genetic models, like gene knockout models, are valuable for studying Tns1 [1].

Tns1-knockout MDCK cells and mouse models have been used to study cystic kidney disease. Tns1-knockout MDCK cells form cysts with multiple lumens and have upregulated Mek/Erk activities. Re-expression of wild-type Tns1, but not a mutant lacking a cell-cell junction localization fragment, can rescue this phenotype. Mek inhibitor treatments can also restore the multiple lumens to single-lumen cysts. In Tns1-knockout mouse kidneys, treatment with the Mek inhibitor trametinib significantly reduces interstitial infiltrates, fibrosis, and dilated tubules, providing potential therapeutic strategies for cystic kidney diseases [2].

In conclusion, Tns1 is crucial for various biological processes, especially those related to cell behavior. Tns1-knockout models have revealed its role in cystic kidney disease, highlighting its potential as a therapeutic target in this disease area. Additionally, its abnormal expression is linked to tumor development, indicating its importance in understanding cancer biology as well [1,2].