Further functional studies suggested that EV-associated MALAT-1 could stimulate tumor growth and migration while suppressing apoptosis in vitro in lung cancer cell lines as corroborated in another study.144 Further, its role in lung cells was examined in vitro and in vivo using knockdown and overexpression models to reveal that MALAT-1 acted as competing endogenous RNA to miR-515-5p, which in turn regulated the Eukaryotic Translation Elongation Factor 2 (EEF2) expression to aid in tumor progression. This evidence concerns the gene MALAT1 and lung cancer.