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p21WAF1/CIP1 gene transcriptional activation exerts cell growth inhibition and enhances chemosensitivity to cisplatin in lung carcinoma cell

Junxia Wei, Jiang Zhao2, Min Long1, Yuan Han1, Xi Wang1, Fang Lin1, Jihong Ren1, Ting He1 and Huizhong Zhang1*

Author Affiliations

1 Department of Clinical Laboratory and Research Center, Tangdu Hospital; Fourth Military Medical University; Xi'an, China

2 Department of Orthopaedics, Xi'an Railway Central Hospital; Xi'an, China

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BMC Cancer 2010, 10:632  doi:10.1186/1471-2407-10-632

Published: 19 November 2010



Non-small-cell lung carcinomas (NSCLCs) exhibit poor prognosis and are usually resistant to conventional chemotherapy. Absence of p21WAF1/CIP1, a cyclin-dependent kinase (cdk) inhibitor, has been linked to drug resistance in many in vitro cellular models. RNA activation (RNAa) is a transcriptional activation phenomena guided by double-strand RNA (dsRNA) targeting promoter region of target gene.


In this study, we explored the effect of up-regulation of p21 gene expression on drug-resistance in A549 non-small-cell lung carcinoma cells by transfecting the dsRNA targeting the promoter region of p21 into A549 cells.


Enhanced p21 expression was observed in A549 cells after transfection of dsRNA, which was correlated with a significant growth inhibition and enhancement of chemosensitivity to cisplatin in A549 cells in vitro. Moreover, in vivo experiment showed that saRNA targeting the promoter region of p21 could significantly inhibit A549 xenograft tumor growth.


These results indicate that p21 plays a role in lung cancer drug-resistance process. In addition, this study also provides evidence for the usage of saRNA as a therapeutic option for up-regulating lower-expression genes in lung cancer.