title: Modulation of E-cadherin expression promotes migration ability of esophageal cancer cells.
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.
authors.affiliation: Department of Thoracic Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang, 050051, China.
authors.forename: Shujun
authors.initials: S
authors.lastname: Li
authors.affiliation: Department of Thoracic Surgery, Hebei Chest Hospital, Shijiazhuang, 050051, China.
authors.forename: Xuebo
authors.initials: X
authors.lastname: Qin
authors.affiliation: Cancer Center, The Second Hospital of Hebei Medical University, Shijiazhuang, 050051, China.
authors.forename: Song
authors.initials: S
authors.lastname: Chai
authors.affiliation: Cancer Center, The Second Hospital of Hebei Medical University, Shijiazhuang, 050051, China.
authors.forename: Changbao
authors.initials: C
authors.lastname: Qu
authors.affiliation: Cancer Center, The Second Hospital of Hebei Medical University, Shijiazhuang, 050051, China.
authors.forename: Xiaolu
authors.initials: X
authors.lastname: Wang
authors.affiliation: Department of Thoracic Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang, 050051, China.
authors.forename: Helin
authors.initials: H
authors.lastname: Zhang
mesh_terms: D000328:Adult; D000368:Aged; D015820:Cadherins / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism; D002294:Carcinoma, Squamous Cell / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D045744:Cell Line, Tumor; D002465:Cell Movement; D002940:Circadian Rhythm / Q000235:genetics*; D004938:Esophageal Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D017930:Genes, Reporter; D056284:Histone Deacetylase 1 / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D008156:Luciferases / Q000235:genetics / Q000378:metabolism; D008207:Lymphatic Metastasis; D008297:Male; D008875:Middle Aged; D056950:Period Circadian Proteins / Q000235:genetics* / Q000378:metabolism; D010957:Plasmids / Q000737:chemistry / Q000378:metabolism; D061251:Primary Cell Culture; D011401:Promoter Regions, Genetic; D034741:RNA, Small Interfering / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D014407:Tumor Cells, Cultured
chemical_list: D015820:Cadherins; C421902:PER2 protein, human; D056950:Period Circadian Proteins; D034741:RNA, Small Interfering; D008156:Luciferases; C110550:HDAC1 protein, human; D056284:Histone Deacetylase 1