CCAAT enhancer binding protein α suppresses proliferation, metastasis, and epithelial-mesenchymal transition of ovarian cancer cells via suppressing the Wnt/ß-catenin signaling.

CCAAT enhancer-binding protein alpha (CEBPA, also known as C/EBPα) is a transcription factor that plays an essential role in regulating terminal differentiation and cell proliferation of many tissues. The objective of this study was to explore the potential function of CEBPA in ovarian cancer. The expression of CEBPA in ovarian cancer samples and adjacent normal tissues was evaluated by qRT-PCR. The putative role of CEBPA in ovarian cancer cells was evaluated by immunohistochemistry, western blot, cell viability assay, BrdU incorporation assay, soft agar colony formation assay, Transwell cell migration and invasion assay, tumor xenograft formation, and lung metastasis model. We found that CEBPA was downregulated in ovarian cancer samples and predicted a poor prognosis. CRISPR/Cas9-mediated CEBPA knockout promoted proliferation, anchorage-independent growth, migration, invasion, and EMT of ovarian cancer cells, while enforced CEPBA expression suppressed proliferation, anchorage-independent growth, migration, invasion, EMT, tumor xenograft growth, and lung metastasis of ovarian cancer cells. Furthermore, we found that the knockout of CEBPA activated Wnt/ß-catenin signaling in ovarian cancer cells, while CEBPA overexpression suppressed Wnt/ß-catenin activation. Our data indicated that CEBPA acted as a tumor suppressor in ovarian cancer, and might be a potential prognostic marker for ovarian cancer treatment.

[Differential expression of extracellular matrix metalloproteinase inducer in normal placenta and preeclampsia placenta].

OBJECTIVE: To study the expression of extracellular matrix metalloproteinase inducer (EMMPRIN) in preeclampsia placenta and the relation with preeclampsia attacks. METHODS: Forty-four samples from pregnant women with preeclampsia (preeclampsia group), 38 samples from pregnant women with eclampsia, and 49 samples from normal pregnancies (control group) were obtained. We detected the expression of EMMPRIN in placenta by immunohistochemistry and the expression of EMMPRIN mRNA by RT-PCR. RESULTS: (1) EMMPRIN positive expression: in preeclampsia group, the moderate expression rate was 18% (8/44) and the strong positive rate was 9% (4/44); in eclampsia group moderate positive rate was 21% (8/38) and strong positive rate 13% (5/38). The difference of the two groups was insignificant (P > 0.05). In control group the moderate positive rate was 12% (6/49) and strong positive rate 82% (40/49), the difference from the preeclampsia and the eclampsia groups was significant (P < 0.001). (2) EMMPRIN mRNA expression: in preeclampsia group EMMPRIN mRNA expression in term placenta (37 - 40 gestational weeks) was 0.342 +/- 0.002, and in eclampsia group 0.344 +/- 0.023; the difference between the two groups was insignificant (P > 0.05). In control group EMMPRIN mRNA expression in term placenta (37 - 40 gestational weeks) was 0.872 +/- 0.094, the differences between the control group and preeclampsia and eclampsia groups were both significant (P < 0.001). CONCLUSION: The decrease in the expression of EMMPRIN in placenta is an important cause of preeclampsia onset; expression rate of EMMPRIN may serve as an indicator in predicting preeclampsia.