title: MiR-622 functions as a tumor suppressor and directly targets E2F1 in human esophageal squamous cell carcinoma.
abstract: OBJECTIVE
  MicroRNA-622 has been proven down-regulated in many human malignancies and correlated with tumor progression. However, its role in esophageal squamous cell carcinoma (ESCC) is still unclear. The aim of this study was to explore the expression and function of miR-622 in ESCC.
  
  
  METHODS
  Using quantitative RT-PCR, we detected miR-622 expression in ESCC cell lines and primary tumor tissues. The association of miR-622 expression with clinicopathological factors and prognosis was also analyzed. Then, the effects of miR-622 on the biological behavior of ESCC cells were investigated. At last, the potential regulatory function of miR-622 on E2F1 expression was confirmed.
  
  
  RESULTS
  miR-622 was found to be down-regulated in ESCC tissues and cell lines. Decreased miR-622 expression was closely correlated with aggressive clinicopathological features and poor overall survival. Multivariate regression analysis corroborated that low level of miR-622 expression was an independent unfavourable prognostic factor for patients with ESCC. Up-regulation of miR-622 could significantly reduce ESCC cell proliferation, enhance cell apoptosis, and impair cell invasion and migration in vitro, while down-regulation of miR-622 showed opposite effects. Further, E2F1 was confirmed as a direct target of miR-622 by using Luciferase Reporter Assay.
  
  
  CONCLUSIONS
  These findings indicate that miR-622 may act as a tumor suppressor in ESCC and would serve as a potential therapy target for this disease.
authors: Department of Thoracic Surgery, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, China.
authors: Changshan
authors: C
authors: Song
authors: Department of Thoracic Surgery, Guangdong General Hospital of Armed Police Forces, Affiliated to Guangzhou Medical University, Guangzhou, Guangdong 510507, China.
authors: Pingfang
authors: P
authors: Lu
authors: Department of Thoracic Surgery, Guangdong General Hospital of Armed Police Forces, Affiliated to Guangzhou Medical University, Guangzhou, Guangdong 510507, China.
authors: Weicheng
authors: W
authors: Shi
authors: Department of Thoracic Surgery, The Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong 524023, China.
authors: Guoqiang
authors: G
authors: Sun
authors: Department of Thoracic Surgery, 2nd Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, Guangdong 518020, China.
authors: Guangsuo
authors: G
authors: Wang
authors: Department of Thoracic Surgery, Guangdong General Hospital of Armed Police Forces, Affiliated to Guangzhou Medical University, Guangzhou, Guangdong 510507, China.
authors: Xujie
authors: X
authors: Huang
authors: Department of Thoracic Surgery, 2nd Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, Guangdong 518020, China. Electronic address: manuwangzheng@163.com.
authors: Zheng
authors: Z
authors: Wang
authors: Department of Thoracic Surgery, The Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong 524023, China. Electronic address: squarelu@163.com.
authors: Zhigang
authors: Z
authors: Wang
mesh_terms: D001483:Base Sequence; D002294:Carcinoma, Squamous Cell / Q000235:genetics* / Q000473:pathology; D045744:Cell Line, Tumor; D050687:E2F1 Transcription Factor / Q000235:genetics / Q000378:metabolism*; D004938:Esophageal Neoplasms / Q000235:genetics* / Q000473:pathology; D000077277:Esophageal Squamous Cell Carcinoma; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D016147:Genes, Tumor Suppressor; D006801:Humans; D053208:Kaplan-Meier Estimate; D008297:Male; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D008875:Middle Aged; D015999:Multivariate Analysis; D011379:Prognosis
chemical_list: D050687:E2F1 Transcription Factor; C493753:E2F1 protein, human; C560103:MIRN622 microRNA, human; D035683:MicroRNAs
keywords: Apoptosis; E2F1; Esophageal squamous cell carcinoma; MiR-622; Prognosis; Proliferation