Digestive Diseases and Sciences

, Volume 58, Issue 12, pp 3483–3493

Down-Regulation of PTEN Expression Modulated by Dysregulated miR-21 Contributes to the Progression of Esophageal Cancer

Original Article

DOI: 10.1007/s10620-013-2854-z

Cite this article as:
Li, P., Mao, WM., Zheng, ZG. et al. Dig Dis Sci (2013) 58: 3483. doi:10.1007/s10620-013-2854-z


Background and Aim

miR-21, a putative tumor oncomiR, is a frequently overexpressed miRNA in a variety of tumors. Because it targets tumor-suppressor genes it has been linked to tumor progression. In this study we investigated the role of miR-21 in esophageal squamous cell carcinoma (ESCC), and its possible mechanism.


Expression of miR-21 was detected by stem–loop RT-PCR in tissue from 76 invasive ESCC at stage I–IV and in their corresponding para-cancerous histological normal tissues (PCHNT). Thirty endoscopic esophageal mucosal biopsy specimens from non-tumor patients were used as controls. Expression of PTEN in 76 paired ESCC and PCHNT was investigated by real-time RT-PCR and an immunohistochemical method, respectively. Paired tumor and PCHNT specimens of 20 ESCC cases were randomly selected for western blot analysis. The effect of miR-21 on PTEN expression was assessed in the ESCC cell line with an miR-21 inhibitor to reduce miR-21 expression. Furthermore, the roles of miR-21 in cell biology were analyzed by use of miR-21 inhibitor-transfected cells.


Stem–loop RT-PCR revealed miR-21 was significantly overexpressed in ESCC tissues and cell lines. Overexpression of miR-21 correlated with tumor status, lymph node metastasis, and clinical stage. We demonstrated that knockdown of miR-21 significantly increased expression of PTEN protein. Consequent PTEN expression reduced cell proliferation, invasion, and migration.


Our findings suggest that miR-21 could be a potential oncomiR, probably by regulation of PTEN, and a novel prognostic factor for ESCC patients.


miR-21 PTEN Stem–loop RT-PCR Esophageal squamous cell carcinoma (ESCC) Progression 

Copyright information

© Springer Science+Business Media New York 2013

Authors and Affiliations

  1. 1.Department of Pathophysiology, School of Basic Medical SciencesZhengzhou UniversityZhengzhouPeople’s Republic of China
  2. 2.Zhejiang Cancer Research Institute, Zhejiang Province Cancer HospitalZhejiang Cancer CenterHangzhouPeople’s Republic of China
  3. 3.Zhejiang Key Laboratory of Diagnosis and Treatment Technology on Thoracic Oncology (Lung and Esophagus)HangzhouPeople’s Republic of China

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