Partition-Defective 3 (PARD3) Regulates Proliferation, Apoptosis, Migration, and Invasion in Esophageal Squamous Cell Carcinoma Cells
Lei Wang, Haiping Zhang, Ayshamgul Hasim, Abuduaini Tuerhong, Zhichao Hou, Ablajan Abdurahmam, Ilyar Sheyhidin
Department of Thoracic Surgery, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China (mainland)
Med Sci Monit 2017; 23:2382-2390
Altered expression of partition-defective 3 (PARD3), a polarity-related gene associated with oncogenesis, has been identified in some cancers, but the role of PARD3 in esophageal squamous cell carcinoma (ESCC) remains unclear.
MATERIAL AND METHODS: PARD3 expression in Eca109 cells was silenced using siRNA and overexpressed using an expression vector. We investigated the role of PARD3 in ESCC growth and motility to evaluate its potential role in ESCC. Transwell assay was used to evaluated cell migration and invasion. PARD3 protein expression was assessed by Western blot.
RESULTS: PARD3 overexpression promoted apoptosis, impaired proliferation, and inhibited cell migration and invasion in Eca109 cells, while PARD3 silencing promoted proliferation and increased migration and invasion. Overexpression of PARD3 exerted its antitumor activity in vitro by impairing cell proliferation, inducing apoptosis, and inhibiting migration and invasion of Eca109 cells, suggesting that PARD3 might play a tumor suppressor role in ESCC.
CONCLUSIONS: Overexpression of PARD3 could be a promising new therapeutic intervention against ESCC.
Keywords: Apoptosis, Carcinoma, Squamous Cell, Cell Migration Assays, Cell Proliferation