Yuan et al. BMC Cancer 2011, 11:57 http://www.biomedcentral.com/1471-2407/11/57 R E S E A R C H A R T I C L E Open Access MicroRNA-203 inhibits cell proliferation by repressing ΔNp63 expression in human esophageal squamous cell carcinoma Yang Yuan1†, Zhi-Yong Zeng2†, Xiao-Hong Liu1†, De-Jun Gong1, Jing Tao3, He-Zhong Cheng3*, Sheng-Dong Huang1* Abstract Background: This study was performed to investigate the effect of microRNA-203 (miR-203) and ΔNp63 on cell proliferation and the functional connection between miR-203 and ΔNp63 in ESCC. Methods: We employed 2 human ESCC cell lines, Eca109 and TE-1, as the model system. The effect of miR-203 and ΔNp63 on cell proliferation was determined in cells transfected with miR-203 mimic and ΔNp63 small interfering RNA (siRNA), respectively. The regulation of ΔNp63 expression in ESCC cells by miR-203 was studied by luciferase reporter assay, RT-PCR and western blot analysis in cells transfected with miR-203. The effect of ΔNp63 re- expression on miR-203 induced inhibition of cell proliferation was studied by cell proliferation assay in cells cotransfected with miR-203 and pcDNA-ΔNp63 plasmid (without the 3’-UTR of ΔNp63). Results: We found that both miR-203 and ΔNp63 siRNA signicantly inhibited cell proliferation in ESCC. MiR-203 could down-regulate endogenous ΔNp63 expression at the posttranscriptional level. Moreover, re-expression of ΔNp63 in cells transfected with miR-203 significantly attenuated the miR-203 induced inhibition of cell proliferation. Conclusions: Our data implied that miR-203 could inhibit cell proliferation in human ESCC through ΔNp63- mediated signal pathway. Therefore, we propose that miR-203 might be used as a therapeutic agent for human ESCC. Background Esophageal cancer is one of the most lethal human cancers mainly located in China, Japan, and southeast Africa [1]. According to the etiologic and pathologic characteristics, it could be divided into two main forms, esophageal squamous cell carcinoma (ESCC) and eso- phageal adenocarcinoma (EAC). Previous reports showed that the incidence of ESCC is much higher than that of EAC in the above mentioned areas [1,2], and the 5-year survival rate of ESCC after surgery ranges from 14% - 22% [3,4]. Much effort has been spent on the study of the biological behavior of ESCC cells to develop * Correspondence: Dr.hezhongCheng@gmail.com; huangsd@smmu.edu.cn † Contributed equally 1Institute of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, PR China 3Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, PR China Full list of author information is available at the end of the article effective treatment strategies. Although some oncogenes and tumor suppressor genes were reported to be asso- ciated with the development of ESCC [5-7], few specific molecules regulating the initiation and progression of ESCC have been identified. Conceivably, elucidation of the molecular pathways involved in the cell proliferation of ESCC will provide important clues for the develop- ment and evaluation of novel anticancer therapies. MicroRNAs, a class of small non-coding RNAs, have been identified as a new kind of gene expression regula- tors through targeting the 3’-untranslated region (UTR) of mRNAs for translational repression, degradation or both [8-10]. In the recent years, mounting data suggest that microRNAs are involved in essential tumor cell bio- logical processes, such as proliferation, invasion, and apoptosis [9,11,12]. It was reported that MicroRNA-203 (miR-203) located in a region at chromosome 14 [13], which contains a © 2011 Yuan et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.