δ-Catenin promotes tumorigenesis and metastasis of lung adenocarcinoma

delta-Catenin coded by gene CTNND2 has been found to be overexpressed in various types of cancers, including prostate, breast, lung and ovarian cancers. However, the function of delta-catenin in lung carcinoma remains largely unknown. In the present study, we revealed that delta-catenin acts as an oncogene promoting the malignancy of lung adenocarcinoma. When delta-catenin proteins of Lewis lung cells were depleted by knocking out Ctnnd2 via CRISPR/Cas9 technology, the cells lost the tumorigenic and metastatic abilities in vivo. Consistently, overexpression of Ctnnd2 enhances the subcutaneous tumorigenesis and distant metastasis of Lewis lung cells in vivo. However, delta-catenin promotes cell proliferation and cell cycle progression of Lewis lung cells. Mechanistically, delta-catenin enhances G1-S phase transition in cooperation with canonical Wnt signaling in Lewis lung cells. Moreover, delta-catenin promotes oncosphere formation of lung adenocarcinoma cells and is associated with the expression of cancer stem cell markers, which indicates delta-catenin enhances colonization and invasion via cancer stem cell maintenance. Taken together, our data suggest that delta-catenin may serve an important role in the malignancy of lung adenocarcinoma through activating canonical Wnt signaling and cancer stem cell maintenance. Our research indicates that delta-catenin can be a new potential target for the treatment of lung adenocarcinoma.