In this study, we found that MALAT1 was downregulated in breast tumor cell lines and cancer tissue, and showed that knockdown of MALAT1 in breast cancer cell lines induced an epithelial-to-mesenchymal transition (EMT) program via phosphatidylinositide-3 kinase-AKT pathways.
Overexpression of MALAT1 has been shown to be positively correlated with tumor progression and metastasis in a large number of tumor types including breast tumors.