Objective   To explore the regulatory mechanism of non-structural maintenance of chromosome condensin I complex submit G (NCAPG) on proliferation, migration, and invasion of ovarian cancer cells.  Methods   The bioinformatics database was used to analyze the differential expression of NCAPG in ovarian cancer tissues. Western blotting was used to detect the protein expression of NCAPG in normal ovarian epithelial cells IOSE80, ovarian cancer A2780 and SKOV3 cells. The silencing experiments of NCAPG siRNA were divided into blank, control, siNCAPG-1 and siNCAPG-2 groups. The overexpression experiments of NCAPG plasmid were divided into blank, control, NCAPG, NCAPG+MK2206 and MK2206 groups. MTT assay was used to detect cell proliferation activity. Cell scoring assay and transwell assay were used to analyze cell migration and invasion. The protein expressions of p-Akt, total(t)-Akt, proliferative cellular nucleus antigen (PCNA), matrix metallopeptidase 9 (MMP-9), vimentin, N-cadherin, and E-cadherin were detected by Western blotting.  Results   NCAPG was highly expressed in ovarian cancer tissues and cells. Knockdown of NCAPG significantly inhibited the proliferation, invasion and migration of ovarian cancer SKOV3 cells. The protein expressions of p-Akt, PCNA, MMP-9, vimentin and N-cadherin decreased while E-cadherin expression increased. Overexpression of NCAPG significantly promoted the proliferation, invasion and migration of ovarian cancer A2780 cells. The protein expressions of pAkt, PCNA, MMP-9, vimentin, and N-cadherin increased while E-cadherin expression decreased. Akt inhibitor MK2206 significantly attenuated the above effects of NCAPG.  Conclusion  NCAPG promotes the proliferation, invasion, and migration of ovarian cancer cells by activating the Akt signaling pathway and regulating the expression of PCNA, MMP-9, and epithelial-mesenchymal transition (EMT)-related proteins.