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J Cancer Res Clin Oncol. 2012 Aug;138(8):1355-61. doi: 10.1007/s00432-012-1194-2. Epub 2012 Apr 7.

Tumor suppressor miR-22 suppresses lung cancer cell progression through post-transcriptional regulation of ErbB3.

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  • 1Key Laboratory of Biological Science and Technology, Chongqing University, Ministry of Education, Bioengineering College of Chongqing University, Chongqing 400044, China.



Development of efficient therapies of lung cancer and deep understanding of their anti-tumor mechanism are very important. The aim of the present study is to investigate the therapeutic effect of microRNA-22 (miR-22) on lung cancer using in vitro and in vivo methods.


Expression level of miR-22 in lung cancer specimens and relative normal tissues was detected by microRNA-specific quantitative real-time PCR (Q-PCR). Invasion assay, cell counting kit-8 assay, and Annexin V/7-AAD analysis were performed to test the invasion and proliferation of lung cancer cell after transfection. The effect of miR-22 on lung cancer in vivo was validated by murine xenograft model.


Q-PCR detection of miR-22 in clinical samples showed that the relative expression level of miR-22 in lung cancer tissues and lung cancer cell lines was lower than that in normal tissues. Transfection of miR-22 expression plasmids could significantly inhibit the increased cell numbers and invasion of A549 and H1299 lung cancer cell lines. Furthermore, miR-22 was demonstrated to inhibit the expression of ErbB3 through post-transcriptional regulation via binding to ErbB3 3'-UTR. Co-transfection of ErbB3 expression plasmid could promote the proliferation and invasion of A549 and H1299. In vivo experiments using nude mice demonstrated that over-expression of miR-22 could significantly decrease the volume and weight of tumors.


miR-22 exhibited excellent anti-lung cancer activity in vitro and in vivo, and post-transcriptional regulation of ErbB3 might be a potential mechanism.

[PubMed - indexed for MEDLINE]
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