PMID- 25333812 OWN - NLM STAT- MEDLINE DCOM- 20150624 LR - 20181202 IS - 1791-3004 (Electronic) IS - 1791-2997 (Linking) VI - 11 IP - 1 DP - 2015 Jan TI - Silencing survivin expression inhibits the tumor growth of non-small-cell lung cancer cells in vitro and in vivo. PG - 639-44 LID - 10.3892/mmr.2014.2729 [doi] AB - Survivin is a promising anticancer therapeutic target due to its important role in the inhibition of apoptosis of tumor cells. However, little is currently known about its role in non small cell lung cancer (NSCLC). The present study evaluated whether the downregulation of survivin expression would affect cell proliferation, cell cycle distribution, apoptosis and colony formation of NSCLC. A recombinant lentiviral small hairpin RNA (shRNA) expression vector, which specifically targeted survivin, was constructed and transfected into the A549 human NSCLC cell line. Quantitative polymerase chain reaction and western blotting were used to determine the mRNA and protein expression levels of survivin, 48 h following the knockdown of survivin expression. Cell proliferation, apoptosis, cell cycle distribution and colony formation were determined following the downregulation of survivin by shRNA. In addition, A549 cells were injected into nude mice, and the effects of shRNA targeting the survivin gene on tumor growth were assessed. Downregulation of survivin expression, using the RNA silencing approach in A549 tumor cells, significantly suppressed the proliferation and colony formation ability of the cells, and induced tumor apoptosis in vitro. The nude mice inoculated with A549 cells developed cancer, and treatment with shRNA targeting survivin markedly inhibited the growth of these cancers, with no obvious side effects. The results of the present study suggest that suppression of survivin expression by RNA interference may induce NSCLC apoptosis, and provide a novel approach for anticancer gene therapy. FAU - Zhang, Kejian AU - Zhang K AD - Department of Thoracic Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China. FAU - Li, Yang AU - Li Y AD - Department of Thoracic Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China. FAU - Liu, Wei AU - Liu W AD - Department of Thoracic Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China. FAU - Gao, Xinliang AU - Gao X AD - Department of Thoracic Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China. FAU - Zhang, Kewei AU - Zhang K AD - Department of Thoracic Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China. LA - eng PT - Journal Article DEP - 20141021 PL - Greece TA - Mol Med Rep JT - Molecular medicine reports JID - 101475259 RN - 0 (BIRC5 protein, human) RN - 0 (Inhibitor of Apoptosis Proteins) RN - 0 (RNA, Small Interfering) RN - 0 (Survivin) RN - EC 3.4.22.- (Caspase 3) RN - EC 3.4.22.- (Caspase 8) SB - IM MH - Animals MH - Apoptosis/genetics MH - Carcinoma, Non-Small-Cell Lung/*genetics/*pathology MH - Caspase 3/metabolism MH - Caspase 8/metabolism MH - Cell Cycle/genetics MH - Cell Line, Tumor MH - Cell Proliferation MH - Disease Models, Animal MH - Female MH - *Gene Silencing MH - Humans MH - Inhibitor of Apoptosis Proteins/*genetics MH - Lung Neoplasms/*genetics/*pathology MH - Mice MH - Neoplastic Stem Cells/metabolism MH - RNA Interference MH - RNA, Small Interfering/genetics MH - Survivin MH - Tumor Burden/genetics MH - Xenograft Model Antitumor Assays EDAT- 2014/10/22 06:00 MHDA- 2015/06/25 06:00 CRDT- 2014/10/22 06:00 PHST- 2014/01/26 00:00 [received] PHST- 2014/09/18 00:00 [accepted] PHST- 2014/10/22 06:00 [entrez] PHST- 2014/10/22 06:00 [pubmed] PHST- 2015/06/25 06:00 [medline] AID - 10.3892/mmr.2014.2729 [doi] PST - ppublish SO - Mol Med Rep. 2015 Jan;11(1):639-44. doi: 10.3892/mmr.2014.2729. Epub 2014 Oct 21.