Regulates Epithelial-Mesenchymal Transition of Choriocarcinoma by Mediating TGF-β1 Expression.

BACKGROUND

(), also known as serine/threonine kinase 26 (), promotes development of several cancers and is found to be highly expressed in the placenta. However, in choriocarcinoma that originated from the placenta, the expression of was undetermined and its mechanism was unknown. In this study, the expression of in choriocarcinoma as well as the underlying mechanism was explored.

PURPOSE

To detect the expression of in patient samples and mechanism of mediating EMT by in choriocarcinoma.

PATIENTS AND METHODS

The metastatic lesions of choriocarcinoma (n=17) and volunteer villus (n=17) were collected to determine expression using immunohistochemistry and H&E staining. We use siRNA and lentiviral vector to knockdown and use plasmid to overexpress in choriocarcinoma. Then, we apply real-time polymerase chain reaction (RT-PCR), Western blot assay and immunofluorescence assay to detect target protein expressions. Cell invasion and migration and cell proliferation were detected by transwell assay and wound healing assay and CCK-8 and cell colony formation.

RESULTS

is lowly expressed in the metastatic lesions of choriocarcinoma patients when compared with normal villus. Knockdown of activated epithelial-mesenchymal transition (EMT) process, significantly increasing the ability of invasion and migration in choriocarcinoma cell lines (JAR and JEG-3). In contrast, the EMT process was restrained in choriocarcinoma cell lines with overexpressed . Meanwhile, genome-wide gene expression array, Western blot and ELISA revealed that tumor growth factor-beta 1 (TGF-β1) has significantly increased. The EMT process and metastatic prompting biofunction were reversed after using TGF-β1 inhibitor (LY364947) in the choriocarcinoma cell lines with knockdown.

CONCLUSION

Our studies demonstrated that was lowly expressed in patient samples. Additionally, JAR and JEG-3 increase cell invasion and migration ability while there is no influence on cell proliferation with knockdown. Conversely, the metastatic ability of JAR and JEG-3 was decreased with overexpressed . Moreover, TGF-β1 was a key factor after knockdown. In conclusion, affects choriocarcinoma EMT by mediating TGF-β1 expression.