Tmprss11e, a transmembrane serine protease, is expressed in epithelial cells. It has been implicated in diverse biological processes, with its upregulation observed in various disease-related contexts. It may be involved in pathways related to inflammation and cancer progression, highlighting its biological importance in understanding disease mechanisms [1,2].

In an LPS-induced acute lung injury mouse model and a cecal ligation and puncture-induced sepsis model, increased Tmprss11e expression was seen in lung tissues. Knockdown of Tmprss11e suppressed pro-inflammatory cytokine release and alleviated lung injury, suggesting its role in promoting pulmonary inflammation [1]. In NSCLC, overexpressing Tmprss11E promoted A549 cell proliferation and migration, while the S372A mutant with a mutated catalytic domain lost this promoting function. Also, silencing Tmprss11e expression inhibited the growth of 95D cell-derived tumors in mouse xenograft models [2].

In conclusion, Tmprss11e is involved in both inflammatory responses and cancer-related processes. Findings from gene-knockout (KO) or conditional-knockout (CKO) equivalent models, such as the knockdown experiments in the lung injury and NSCLC models, have revealed its role in promoting pulmonary inflammation and NSCLC progression. This understanding can contribute to developing therapeutic strategies for related diseases [1,2].