Abstract
Losing the E-cadherin plays an important role in the metastasis of cancer. The regulation of the expression of E-cadherin is unclear. Circadian rhythm alteration is associated with the pathogenesis of a number of cancers. This study aims to investigate the role of one of the circadian proteins, period-2 (Per2) in repressing the expression of E-cadherin in esophageal cancer (esophageal cancer). We observed that the levels of circadian protein Per2 were significantly increased and E-cadherin was significantly decreased in the tissue of human esophageal cancer with metastasis as compared with non-metastatic esophageal cancer. Overexpression of Per2 in the esophageal cancer cells markedly repressed the expression of E-cadherin. The pHDAC1 was detected in human esophageal cancer with metastasis, which was much less in the esophageal cancer tissue without metastasis. Overexpression of Per2 increased the levels of pHDAC1 as well as the E-cadherin repressors at the E-cadherin promoter locus. Overexpression of Per2 markedly increased the migratory capacity of esophageal cancer cells, which was abolished by the inhibition of HDAC1. We conclude that Per-2 plays an important role in the esophageal cancer cell metastasis, which may be a novel therapeutic target for the treatment of esophageal cancer.
Highlights
We wondered if the circadian clock disruption was associated with esophageal cancer metastasis
The esophageal cancer cells were negatively isolated by magnetic cell sorting (MACS) and subjected to Real time quantitative RT-PCR (RT-qPCR) to detect the expression of circadian clock molecule mRNA, including NFIL3, Per[1], Per[2], Bmal[1], Cry[1], Cry[2], Clock and Npas[2]
Since a decrease in E-cadherin is an important factor in the pathogenesis of cancer metastasis[11], we assessed the expression of E-cadherin in the esophageal cancer cells and the marginal tissue
Summary
Results Expression of Per[2] and E-cadherin was detected in esophageal cancer with metastasis. The results showed that the expression of E-cadherin was markedly less in esophageal cancer with metastasis that of the esophageal cancer without metastasis and the marginal tissue (Fig. 1B). Per[2] represses the expression of E-cadherin in esophageal cancer cells.
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