Abstract
Increasing evidence has suggested that mitochondrial calcium uniporter (MCU) is involved in various types of cancer. However, its functions remain unclear in esophageal cancer. The aim of the present study was to explore its abnormal expression and clinical implications in esophageal cancer. A total of 110 patients with esophageal cancer were enrolled in the study. Western blotting was performed to examine the protein expression levels of MCU in 8 pairs of esophageal cancer and adjacent normal tissues. Using immunochemistry, a total of 110 esophageal cancer specimens were analyzed to identify the association between MCU expression and clinicopathological features of patients with esophageal cancer. Furthermore, immunofluorescence of MCU was performed. Pearson's correlation analysis was performed between MCU and hypoxia inducible factor (HIF)-1α/VEGF/E-cadherin/Vimentin expression based on western blotting. After KYSE-150 and TE-1 cells were treated with the MCU agonist Spermine and a small interfering RNA against MCU (si-MCU), a series of functional assays were performed, including Cell Counting Kit-8, colony formation and Transwell assays. The results revealed that, compared with in adjacent normal tissues, MCU was highly expressed in esophageal cancer tissues. MCU expression was significantly associated with depth of invasion, lymph node metastasis, TNM stage and distant metastasis. Moreover, MCU was significantly correlated with HIF-1α/VEGF/E-cadherin/Vimentin in esophageal cancer tissues. MCU overexpression promoted VEGF, MMP2, Vimentin and N-cadherin expression, while it inhibited E-cadherin expression in KYSE-150 and TE-1 cells, and opposite results were observed after transfection with si-MCU. Furthermore, MCU overexpression accelerated the proliferation and migration of KYSE-150 and TE-1 cells. Thus, the current findings suggested that high MCU expression may participate in cell proliferation, migration and epithelial-mesenchymal transition in esophageal cancer.