Our results indicate that the long noncoding RNA MALAT1 could sponge miR-211 as a competing endogenous RNA and potentially up-regulate PHF19 expression, thus facilitating the OC progression. These findings suggest that the MALAT1/miR-211/PHF19 axis may act as a key mediator in OC and provide new insight into the prevention of this disease. MALAT1 expression was up-regulated in OC tissues compared with normal ovarian tissues. A significant positive correlation was noted between MALAT1 and PHF19 . Meanwhile, TCGA cohort analysis showed that higher expression of MALAT1 was correlated with shorter survival times for patients with OC. To confirm the role of MALAT1 in OC, we further knocked down the expression of MALAT1 in SKOV3 cells . The results show that silence of MALAT1 significantly inhibited cell proliferation and colony formation ability in SKOV3 cells. Moreover, an increasing number of apoptotic cells were observed in MALAT1- silenced SKOV3 cells . In addition, silence of MALAT1 also dramatically suppressed the migration of SKOV3 cells. In vivo, the xenograft experiment showed that infection with MALAT1 shRNA lentivirus in SKOV3 cells significantly reduced the tumor growth rate. These data suggest that MALAT1 may be an oncogenic lncRNA in OC.