MicroRNA-203 inhibits cell proliferation by repressing ΔNp63 expression in human esophageal squamous cell carcinoma
Autor: | Xiaohong Liu, Zhi-Yong Zeng, Shengdong Huang, Yang Yuan, Dejun Gong, Jing Tao, He-Zhong Cheng |
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Rok vydání: | 2011 |
Předmět: |
Cancer Research
Esophageal Neoplasms Blotting Western Biology lcsh:RC254-282 Surgical oncology RNA interference Cell Line Tumor microRNA Genetics Humans Doubling time Luciferases 3' Untranslated Regions Transcription factor Cell Proliferation Reverse Transcriptase Polymerase Chain Reaction Three prime untranslated region Cell growth Tumor Suppressor Proteins lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens Molecular biology Gene Expression Regulation Neoplastic MicroRNAs Oncology Carcinoma Squamous Cell Trans-Activators Cancer research RNA Interference Stem cell Transcription Factors Research Article |
Zdroj: | BMC Cancer, Vol 11, Iss 1, p 57 (2011) BMC Cancer |
ISSN: | 1471-2407 |
DOI: | 10.1186/1471-2407-11-57 |
Popis: | 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. |
Databáze: | OpenAIRE |
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