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Tumor suppressor in lung cancer-1 (TSLC1) mediated by dual-regulated oncolytic adenovirus exerts specific antitumor actions in a mouse model

Aim: The tumor suppressor in lung cancer-1 (TSLC1) is a candidate tumor suppressor of lung cancer, and frequently inactivated in primary non-small cell lung cancer (NSCLC). In this study, we investigated the effects of TSLC1 mediated by a dual-regulated oncolytic adenovirus on lung cancer, and the m... Full description

Journal Title: Acta pharmacologica Sinica 2013 (4), p.531-540
Main Author: Wen LEI Hong-bin LIU Shi-bing WANG Xiu-mei ZHOU Shui-di ZHENG Ke-ni GUO Bu-yun MA Yu-Iong XIA Wen-song TAN Xin-yuan LIU Yi-gang WANG
Format: Electronic Article Electronic Article
Language: English
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ID: ISSN: 1671-4083
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recordid: cdi_chongqing_primary_45518998
title: Tumor suppressor in lung cancer-1 (TSLC1) mediated by dual-regulated oncolytic adenovirus exerts specific antitumor actions in a mouse model
format: Article
creator:
  • Wen LEI Hong-bin LIU Shi-bing WANG Xiu-mei ZHOU Shui-di ZHENG Ke-ni GUO Bu-yun MA Yu-Iong XIA Wen-song TAN Xin-yuan LIU Yi-gang WANG
subjects:
  • Caspase
  • caspase-3
  • survivin
  • 抗肿瘤作用
  • 肿瘤抑制
  • 腺病毒介导
  • 非小细胞肺癌
ispartof: Acta pharmacologica Sinica, 2013 (4), p.531-540
description: Aim: The tumor suppressor in lung cancer-1 (TSLC1) is a candidate tumor suppressor of lung cancer, and frequently inactivated in primary non-small cell lung cancer (NSCLC). In this study, we investigated the effects of TSLC1 mediated by a dual-regulated oncolytic adenovirus on lung cancer, and the mechanisms underlying the antitumor actions. Methods: The recombinant virus Ad.sp-E1A(△24)-TSLC1 was constructed by inserting the TSLC1 gene into the dual-regulated Ad.sp- E/A(△24) vector, which contained the survivin promoter and a 24 bp deletion within EIA. The antitumor effects of Ad.sp-EIA/(△24)-TSLC1 were evaluated in NCI-H460, A549, and H1299 lung cancer cell lines and the normal fibroblast cell line MRC-5, as well as in A549 xenograft model in nude mice. Cell viability was assessed using MTT assay. The expression of TSLC1 and activation of the caspase signaling pathway were detected by Western blot analyses. The tumor tissues from the xenograft models were examined using H&E staining, IHC, TUNEL, and TEM analyses. Results: Infection of A549 lung cancer cells with Ad.sp-E1A(△24)-TSLC1 induced high level expression of TSLC1. Furthermore, the Ad.sp- E/A(△24)-TSLC1 virus dose-dependently suppressed the viability of NCI-H460, A549, and H1299 lung cancer cells, and did not affect MRC-5 normal fibroblast cells. Infection of NCI-H460, A549, and H1299 lung cancer cells with Ad-sp-E1A(△24)-TSLCl induced apoptosis and increased activation of caspase-8, caspase-3 and PARP. In A549 xenograft model in nude mice, intratumoral injection of Ad.sp- E/A(△24)-TSLC1 significantly suppressed the tumor volume, and increased the survival rate (from less than 15% to 87.5% at d 60). Histological studies showed that injection of Ad.sp-EIA(△24)-TSLC1 caused tumor cell apoptosis and virus particle propagation in tumor tissues. Conclusion: The oncolytic adenovirus Ad-sp-E1A(△24)-TSLC1 exhibits specific antitumor effects, and is a promising agent for the treatment of lung cancer.
language: eng
source:
identifier: ISSN: 1671-4083
fulltext: no_fulltext
issn:
  • 1671-4083
  • 1745-7254
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titleTumor suppressor in lung cancer-1 (TSLC1) mediated by dual-regulated oncolytic adenovirus exerts specific antitumor actions in a mouse model
creatorWen LEI Hong-bin LIU Shi-bing WANG Xiu-mei ZHOU Shui-di ZHENG Ke-ni GUO Bu-yun MA Yu-Iong XIA Wen-song TAN Xin-yuan LIU Yi-gang WANG
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descriptionAim: The tumor suppressor in lung cancer-1 (TSLC1) is a candidate tumor suppressor of lung cancer, and frequently inactivated in primary non-small cell lung cancer (NSCLC). In this study, we investigated the effects of TSLC1 mediated by a dual-regulated oncolytic adenovirus on lung cancer, and the mechanisms underlying the antitumor actions. Methods: The recombinant virus Ad.sp-E1A(△24)-TSLC1 was constructed by inserting the TSLC1 gene into the dual-regulated Ad.sp- E/A(△24) vector, which contained the survivin promoter and a 24 bp deletion within EIA. The antitumor effects of Ad.sp-EIA/(△24)-TSLC1 were evaluated in NCI-H460, A549, and H1299 lung cancer cell lines and the normal fibroblast cell line MRC-5, as well as in A549 xenograft model in nude mice. Cell viability was assessed using MTT assay. The expression of TSLC1 and activation of the caspase signaling pathway were detected by Western blot analyses. The tumor tissues from the xenograft models were examined using H&E staining, IHC, TUNEL, and TEM analyses. Results: Infection of A549 lung cancer cells with Ad.sp-E1A(△24)-TSLC1 induced high level expression of TSLC1. Furthermore, the Ad.sp- E/A(△24)-TSLC1 virus dose-dependently suppressed the viability of NCI-H460, A549, and H1299 lung cancer cells, and did not affect MRC-5 normal fibroblast cells. Infection of NCI-H460, A549, and H1299 lung cancer cells with Ad-sp-E1A(△24)-TSLCl induced apoptosis and increased activation of caspase-8, caspase-3 and PARP. In A549 xenograft model in nude mice, intratumoral injection of Ad.sp- E/A(△24)-TSLC1 significantly suppressed the tumor volume, and increased the survival rate (from less than 15% to 87.5% at d 60). Histological studies showed that injection of Ad.sp-EIA(△24)-TSLC1 caused tumor cell apoptosis and virus particle propagation in tumor tissues. Conclusion: The oncolytic adenovirus Ad-sp-E1A(△24)-TSLC1 exhibits specific antitumor effects, and is a promising agent for the treatment of lung cancer.
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0Aim: The tumor suppressor in lung cancer-1 (TSLC1) is a candidate tumor suppressor of lung cancer, and frequently inactivated in primary non-small cell lung cancer (NSCLC). In this study, we investigated the effects of TSLC1 mediated by a dual-regulated oncolytic adenovirus on lung cancer, and the mechanisms underlying the antitumor actions. Methods: The recombinant virus Ad.sp-E1A(△24)-TSLC1 was constructed by inserting the TSLC1 gene into the dual-regulated Ad.sp- E/A(△24) vector, which contained the survivin promoter and a 24 bp deletion within EIA. The antitumor effects of Ad.sp-EIA/(△24)-TSLC1 were evaluated in NCI-H460, A549, and H1299 lung cancer cell lines and the normal fibroblast cell line MRC-5, as well as in A549 xenograft model in nude mice. Cell viability was assessed using MTT assay. The expression of TSLC1 and activation of the caspase signaling pathway were detected by Western blot analyses. The tumor tissues from the xenograft models were examined using H&E staining, IHC, TUNEL, and TEM analyses. Results: Infection of A549 lung cancer cells with Ad.sp-E1A(△24)-TSLC1 induced high level expression of TSLC1. Furthermore, the Ad.sp- E/A(△24)-TSLC1 virus dose-dependently suppressed the viability of NCI-H460, A549, and H1299 lung cancer cells, and did not affect MRC-5 normal fibroblast cells. Infection of NCI-H460, A549, and H1299 lung cancer cells with Ad-sp-E1A(△24)-TSLCl induced apoptosis and increased activation of caspase-8, caspase-3 and PARP. In A549 xenograft model in nude mice, intratumoral injection of Ad.sp- E/A(△24)-TSLC1 significantly suppressed the tumor volume, and increased the survival rate (from less than 15% to 87.5% at d 60). Histological studies showed that injection of Ad.sp-EIA(△24)-TSLC1 caused tumor cell apoptosis and virus particle propagation in tumor tissues. Conclusion: The oncolytic adenovirus Ad-sp-E1A(△24)-TSLC1 exhibits specific antitumor effects, and is a promising agent for the treatment of lung cancer.
1lung cancer; tumor suppressor in lung cancer-I; oncolytic adenovirus; survivin; apoptosis; caspase signaling pathway; tumor xenograft model
231-1347/R
abstractAim: The tumor suppressor in lung cancer-1 (TSLC1) is a candidate tumor suppressor of lung cancer, and frequently inactivated in primary non-small cell lung cancer (NSCLC). In this study, we investigated the effects of TSLC1 mediated by a dual-regulated oncolytic adenovirus on lung cancer, and the mechanisms underlying the antitumor actions. Methods: The recombinant virus Ad.sp-E1A(△24)-TSLC1 was constructed by inserting the TSLC1 gene into the dual-regulated Ad.sp- E/A(△24) vector, which contained the survivin promoter and a 24 bp deletion within EIA. The antitumor effects of Ad.sp-EIA/(△24)-TSLC1 were evaluated in NCI-H460, A549, and H1299 lung cancer cell lines and the normal fibroblast cell line MRC-5, as well as in A549 xenograft model in nude mice. Cell viability was assessed using MTT assay. The expression of TSLC1 and activation of the caspase signaling pathway were detected by Western blot analyses. The tumor tissues from the xenograft models were examined using H&E staining, IHC, TUNEL, and TEM analyses. Results: Infection of A549 lung cancer cells with Ad.sp-E1A(△24)-TSLC1 induced high level expression of TSLC1. Furthermore, the Ad.sp- E/A(△24)-TSLC1 virus dose-dependently suppressed the viability of NCI-H460, A549, and H1299 lung cancer cells, and did not affect MRC-5 normal fibroblast cells. Infection of NCI-H460, A549, and H1299 lung cancer cells with Ad-sp-E1A(△24)-TSLCl induced apoptosis and increased activation of caspase-8, caspase-3 and PARP. In A549 xenograft model in nude mice, intratumoral injection of Ad.sp- E/A(△24)-TSLC1 significantly suppressed the tumor volume, and increased the survival rate (from less than 15% to 87.5% at d 60). Histological studies showed that injection of Ad.sp-EIA(△24)-TSLC1 caused tumor cell apoptosis and virus particle propagation in tumor tissues. Conclusion: The oncolytic adenovirus Ad-sp-E1A(△24)-TSLC1 exhibits specific antitumor effects, and is a promising agent for the treatment of lung cancer.