Abstract:
:Cervical cancer is the second most common gynecological malignancy. The mechanisms of the genesis and progression of cervical cancer are complicated and not thoroughly understood. DEK is reported as an oncogene in various cancers, such as acute myeloid leukemia, bladder cancer, breast cancer and hepatocellular cancer. However, its role in cervical cancer has not been well studied. In our study, we confirmed the DEK protein as an oncoprotein in cervical cancer tissues which is correlated to cervical cancer FIGO staging and tumor type. Moreover, in vitro loss of DEK inhibited cervical cancer cell proliferation, migration and invasion. We proved that silencing DEK downregulated Wnt/β-catenin and MMP-9, and silencing DEK increased GSK-3β activity via regulating its phosphorylation instead of translation. Silencing DEK reduced p-Ser9-GSK-3β and increased p-Tyr216-GSK-3β, which resulted in β-catenin degradation. Finally, the xenograft model in nude mice proved that silencing DEK impaired cervical cancer cell tumorigenicity. This research unveiled the function of DEK in tumorigenesis and metastasis via the DEK/p-Ser9-GSK-3β/p-Tyr216-GSK-3β/β-catenin axis in cervical cancer and gave insights into DEK-targeting therapy for patients suffering from cervical cancer.
journal_name
Oncol Repjournal_title
Oncology reportsauthors
Xu X,Zou L,Yao Q,Zhang Y,Gan L,Tang Ldoi
10.3892/or.2017.5721subject
Has Abstractpub_date
2017-08-01 00:00:00pages
1035-1042issue
2eissn
1021-335Xissn
1791-2431journal_volume
38pub_type
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