Such enhanced expression of epithelial-associated proteins and cell–cell interaction may also explain the reduction of cell migration and invasion properties of the ΔITGA2 cells which is also support by recent studies showing that silencing ITGA2 restored E-cadherin expression and downregulated mesenchymal marker in chemo-resistant gastric cancer cells (Wang et al., 2020) as well as exosome-mediated transfer of ITGA2 in prostate cancer cells (Gaballa et al., 2020). This evidence concerns the gene CDH1 and prostate cancer.