δ-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 δ-catenin in lung carcinoma remains largely unknown. In the present study, we revealed that δ-catenin acts as an oncogene promoting the malignancy of lung adenocarcinoma. When δ-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, δ-catenin promotes cell proliferation and cell cycle progression of Lewis lung cells. Mechanistically, δ-catenin enhances G1-S phase transition in cooperation with canonical Wnt signaling in Lewis lung cells. Moreover, δ-catenin promotes oncosphere formation of lung adenocarcinoma cells and is associated with the expression of cancer stem cell markers, which indicates δ-catenin enhances colonization and invasion via cancer stem cell maintenance. Taken together, our data suggest that δ-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 δ-catenin can be a new potential target for the treatment of lung adenocarcinoma.