J Cancer 2018; 9(20):3743-3754. doi:10.7150/jca.22418 This issue Cite
Research Paper
1. Department of Gynecology, Obstetrics and Gynecology Hospital of Fudan University, Shanghai, 200032, China.
2. Shanghai Key Laboratory of Female Reproductive Endocrine-Related Disease of Fudan University, Shanghai, 200011, China.
3. Department of Pathology, Obstetrics and Gynecology Hospital of Fudan University, Shanghai, 200011, China.
4. Department of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
5. Department of Obstetrics and Gynecology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Background: Human paired box 2 (PAX2) plays a key role in cell fate, early patterning and organogenesis.
Methods: We investigated the function of PAX2 on the biological behavior of endometrial cancer in vitro and in vivo and to explore the regulation mechanism, stable knocking-down and over-expression PAX2 endometrial cancer cell lines were established. CCK-8 and transwell assays were applied to determine proliferation, invasion and migration ability. Cell cycle distribution was analyzed by flow cytometry. Affymetrix GeneChip® human Exon 1.0 ST arrays was used to screen the downstream target genes of PAX2.
Results: PAX2 significantly enhanced proliferation and invasiveness. In addition, PAX2 influenced the expression of cyclin-dependent kinase 1(CDK1), which play pivotal roles in cell cycle pathway. When CDK1 was knocked down, and the cell proliferation promotion role of PAX2 was attenuated dramatically to a level comparable with the control groups.
Conclusions: PAX2, though influencing the expression of CDK1, promotes the proliferation, enhances the mobility of endometrial cancer cells, thus exerts an important role in the carcinogenesis of endometrial cancer. PAX2 may be a potential therapeutic target for endometrial cancer.
Keywords: PAX2, Ovarian cancer, Cell proliferation