〔Abstract〕 Objective To explore the mechanism of PVT1 aggravating the malignant biological behavior of cervical cancer cells. Methods shRNA was designed to interfere with PVT1, and then SiHa cells were transfected with sh-PVT1 either alone or with miR-484 inhibitor. The expression levels of PVT1 and mir-484 were detected by fluorescence quantification. The luciferase reporter assay confirmed the targeting relationship between PVT1 and miR-484. The effect of PVT1 on cell growth was detected by BrdU staining. The invasion and migration abilities were detected by Transwell and wound healing assay. The expression of proliferation, invasion and migration related proteins and phosphorylation of p38 MAPK were detected by Western blot. The translocation of p38 to nuclei was imaged by immunofluorescence. Results sh-PVT1 significantly decreased the expression of PVT1 in cervical cancer cells(P<0.05) and promoted the expression of miR-484(P<0.05). The luciferase reporter assay indicated that there was miR-484 binding site on PVT1. Interference with PVT1 significantly inhibited the proliferation of cervical cancer cells and the protein expression levels of Ki67 and proliferating cell nuclear antigen(PCNA)(P<0.05). Meanwhile, sh-PVT1 significantly inhibited the invasion and migration of cervical cancer cells and the protein expression of vascular endothelial growth factor(VEGF), matrix metalloproteinase-9(MMP-9) and E-cadherin, and significantly enhanced the expression of N-cadherin protein(P<0.05). In addition, inhibition of miR-484 expression significantly attenuated the inhibitory effect of sh-PVT1 on invasion, migration and epithelial-mesenchymal transition(EMT) of cervical cancer cells(P<0.05). Conclusion PVT1 can promote the growth, movement and EMT of cervical cancer cells by interfering with miR-484, and induce the activation of p38 MAPK pathway, thereby aggravating the malignant biological behavior of cervical cancer cells.