Tns1, also known as tensin 1, is a member of the tensin family of cellular-adhesion constituents. It engages in multiple biological processes such as cell adhesion, polarization, migration, invasion, proliferation, apoptosis, and mechano-transduction by interacting with various partner proteins. The abnormal expression of Tns1 is associated with the development of various diseases, especially tumors [1].

In Tns1-knockout mice, they develop cystic kidneys and die from renal failure. Tns1-knockout MDCK cells form cysts with multiple lumens and have upregulated Mek/Erk activities. Re-expression of wild-type Tns1 can rescue this phenotype, and treatment with the Mek inhibitor trametinib can reduce interstitial infiltrates, fibrosis, and dilated tubules in Tns1-knockout kidneys, indicating Tns1's role in suppressing Mek/Erk signaling and maintaining lumenogenesis [2].

In conclusion, Tns1 is crucial for normal cell functions and is involved in various biological processes. The Tns1-knockout mouse model has revealed its significance in preventing cystic kidney diseases by suppressing the Mek/Erk pathway. Additionally, its abnormal expression is related to tumor development, highlighting its importance in understanding disease mechanisms [1,2].