affects the biological functions of ovarian cancer cells and induces an antitumor immune response by activating dendritic cells.

BACKGROUND

Ovarian cancer is the 5 most common lethal gynecological malignancy with a 5-year survival rate of about 47% and a localized stage diagnosis of 15%, leading to about 125,000 global deaths each year. Therefore, it is urgent to explore novel and effective strategies for radical cure.

METHODS

Short hairpin RNA targeting the () gene was used to establish knockdown in ovarian cancer cells. RT-PCR was performed to quantify the expression of mRNA, and western blotting was performed to detect the expression of and epithelial-mesenchymal transition-related proteins. Cell counting kit 8 (CCK8) wound healing and transwell assays were performed to assess cell proliferation and cell invasion. Flow cytometry was used to detect CD80-, CD83-, and CD86-expressing dendritic cells (DCs) and cytotoxic T lymphocytes (CTLs) activated by -pulsed DCs.

RESULTS

In this study, we identified as a novel target antigen for immunotherapy against ovarian cancer, which was significantly up regulated in ovarian cancer cells and high-grade ovarian serous adenocarcinoma tissues. knockdown in Ovcar3 cells using short hairpin RNA targeting the gene suppressed the proliferation of migration, invasion, epithelial-mesenchymal transition (EMT), and PI3K/Akt signaling pathway in Ovcar3 cells markedly. significantly up-regulated CD80, CD83, and CD86 (mature makers) expression in DCs and T-cell transformation into CD8 T-cells detected by Flow cytometry.

CONCLUSIONS

For malignant ovarian cancer, overexpression promoted cell proliferation, migration, and invasion via the PI3K/AKT signaling pathway. pulsing mediated DC maturation and activated CTL response . Our study offers promising DC-based immunotherapy of considerable clinical value for patients with ovarian cancer.