Original Article
FOXC2 is overexpressed and participates in cell proliferation in ovarian cancer
Abstract
Background: Forkhead box protein C2 (FOXC2) is an epithelial-to-mesenchymal transition (EMT)—inducing transcription factor and involved in several cancer developments. In this study, we aimed to investigate the role of FOXC2 in ovarian cancer.
Methods: A total of 13 ovarian tissues (11 cases of epithelial ovarian cancer, one case of borderline serous cystadenoma and one case of normal ovarian tissue) were collected and tissue specimens were stained to detect the expression and location of FOXC2 in ovarian cancer by immunohistochemistry. Then shRNAs targeting FOXC2 mRNA were designed to construct FOXC2-shRNA-expressing lentiviral vector (LV- FOXC2). Real-time RT-PCR and western blot assays were conducted to examine the interference effects of shRNA to FOXC2. Additionally, cell counting kit-8 (CCK8) was performed to detect cell proliferation of ID8 cells (mouse ovarian cancer cell) infected with FOXC2-shRNA-lentivirus.
Results: No expression of FOXC2 was found in normal ovarian tissue and a large number of FOXC2 positive cells were found in borderline serous cystadenoma and ovarian cancer tissues including vascular endothelial cells, and FOXC2 was mainly seen in nucleus of ovarian cancer cells. Interference lentivirus of FOXC2 was successfully constructed with the virus titers of 1.2×108~1.3×108 Tu/mL, which significantly decreased the mRNA and protein expression levels of FOXC2 (P<0.05). Furthermore, cell proliferation was significantly suppressed with a time-dependent effect in ID8 cells infected with FOXC2-shRNA-lentivirus.
Conclusions: This study might help to understand the molecular mechanism of FOXC2 in ovarian cancer and provide theoretical foundation for the development of diagnosis and treatment for ovarian cancer by targeting FOXC2.
Methods: A total of 13 ovarian tissues (11 cases of epithelial ovarian cancer, one case of borderline serous cystadenoma and one case of normal ovarian tissue) were collected and tissue specimens were stained to detect the expression and location of FOXC2 in ovarian cancer by immunohistochemistry. Then shRNAs targeting FOXC2 mRNA were designed to construct FOXC2-shRNA-expressing lentiviral vector (LV- FOXC2). Real-time RT-PCR and western blot assays were conducted to examine the interference effects of shRNA to FOXC2. Additionally, cell counting kit-8 (CCK8) was performed to detect cell proliferation of ID8 cells (mouse ovarian cancer cell) infected with FOXC2-shRNA-lentivirus.
Results: No expression of FOXC2 was found in normal ovarian tissue and a large number of FOXC2 positive cells were found in borderline serous cystadenoma and ovarian cancer tissues including vascular endothelial cells, and FOXC2 was mainly seen in nucleus of ovarian cancer cells. Interference lentivirus of FOXC2 was successfully constructed with the virus titers of 1.2×108~1.3×108 Tu/mL, which significantly decreased the mRNA and protein expression levels of FOXC2 (P<0.05). Furthermore, cell proliferation was significantly suppressed with a time-dependent effect in ID8 cells infected with FOXC2-shRNA-lentivirus.
Conclusions: This study might help to understand the molecular mechanism of FOXC2 in ovarian cancer and provide theoretical foundation for the development of diagnosis and treatment for ovarian cancer by targeting FOXC2.
