Cervical cancer (CC) is a common malignant gynecological cancer that is frequently diagnosed in women. Apparently, long noncoding RNA nuclear-enriched autosomal transcript 1 (NEAT1) has been identified as a tumor promoter in multiple cancers. Our research is focused on the effects of lncRNA NEAT1 on cell progression in cervical cancer and the potential molecular mechanism of NEAT1 for CC cell progression. The levels of NEAT1, MicroRNA (miR)-889-3p and E2F transcription factor 7 (E2F7) in CC tumors and cells were measured by a quantitative real-time polymerase chain reaction (qRT-PCR). The interaction of miR-889-3p with NEAT1 and E2F7 was validated by a luciferase reporter system and a RNA immunoprecipitation (RIP) assay, respectively. Cell counting kit-8 (CCK-8) and flow cytometry were used for cell proliferation and apoptosis evaluation. Cell migration and invasion were examined by a transwell assay. The protein expressions of E2F7, AKT, phospho-AKT (p-AKT), phosphatidylinositol 3-kinase (PI3K) and phosphorylated PI3K (p-PI3K) were analyzed by western blot assay. Animal models were established by subcutaneously injecting the Me180 cells stably transfected with sh-NEAT1 and sh-NC. The expressions of NEAT1 and E2F7 were up-regulated, whereas the expression of miR-889-3p was down-regulated in the CC tumors and cells when compared with those in normal tumors and cells. The interaction between miR-889-3p and NEAT1 or E2F7 was proved by luciferase reporter system and RIP assay. In addition, the miR-889-3p inhibitor attenuated the NEAT1 silencing-induced inhibition effects on cell proliferation, migration, and invasion and the promotion effects on apoptosis in CC. Consistently, E2F7 reversed the miR-889-3p-mediated inhibition on cell progression in CC. Moreover, NEAT1 modulated cell behavior by targeting the miR-889-3p/E2F7 axis through the PI3K/AKT pathway. Finally, the intervention of NEAT1 hindered tumor growth in vivo. Thus, NEAT1 contributes to cell progression in CC by targeting miR-889-3p to facilitate the E2F7 expression through the activation of the PI3K/AKT pathway, representing an alternative targeted therapy of CC.