Abstract
Background: S100A14 is involved in multiple pathological processes; however, its role in nasopharyngeal carcinoma is poorly understood. Methods: S100A14 was deleted or upregulated in 6-10B cells. Results: S100A14-knockdown 6-10B cells showed significantly higher optical density values in the CCK-8 assay, smaller scratch width in the scratch experiment, and significantly more invading cells in the transwell assay compared with controls. Compared with the control group, the G2/M and S phase proportions of the S100A14-overexpression group were significantly higher, early apoptosis was observed via JC-1 fluorescence, and flow cytometry showed a significantly higher proportion of apoptotic cells. Protein expression of Bcl-2 and Bcl-xl decreased significantly, whereas that of Bax, Bad, cleaved-PARP, and cleaved-caspase-3/9 increased. Conclusions: Knockdown of S100A14 promoted proliferation, migration, and invasion of 6-10B cells, whereas its upregulation promoted caspase-dependent apoptosis and induced S and G2/M phase arrest, indicating a role of S100A14 as a tumor suppressor gene in nasopharyngeal carcinoma.