Abstract

Highlights:

1. Expression of CDK1 and Sox2 was correlated with esophageal cancer.
2. CDK1 promoted the migration and invasion of ECA109 cells.
3. CDK1 knockdown inhibited phosphorylation and nuclear localization of Sox2

Background: Esophageal carcinoma is an aggressive malignancy characterized with early metastasis and low 5-year survival rate. Cyclin-dependent kinase 1 (CDK1) is a regulator of cell cycle that also contributes to cell proliferation, migration, invasion and drug resistance in multiple cancers. In this study, we aim to explore the role of CDK1 in the malignant phenotype of esophageal carcinoma and its underlying mechanism.

Methods: The expression of CDK1 and SRY-box transcription factor 2 (Sox2) in vivo were analyzed from data mined from GEPIA. Cell migration and invasion ability were analyzed by cell migration assay and transwell invasion assay. The protein and mRNA levels of indicated genes were detected by western blot and RT-qPCR. Protein to protein interaction was detected by immunoprecipitation.

Results: It was found that CDK1 expression was up-regulate in esophageal carcinoma and facilitated cell migration and invasion in vitro. Molecularly, we showed that CDK1 directly interacted with transcriptional factor Sox2, which was also up-regulated in esophageal carcinoma from GEPIA database. CDK1 knockdown inhibited the phosphorylation of Sox2 and facilitated its translocation from nucleus to cytoplasm.

Conclusion: These findings indicate that CDK1-mediated phosphorylation and nuclear localization of Sox2 plays a crucial role in the malignant phenotype in carcinoma and proposes CDK1 as a potential target in the clinical treatment of esophageal carcinoma.

Keywords: Cell migration; Cell invasion; CDK1; Sox2; Esophagealcarcinoma