The levels of integrin αvβ5 may predict the susceptibility to adenovirus-mediated gene transfer in human lung cancer cells

Takayama, K.; Ueno, Hikaru; Pei, Xin-Hai; Nakanishi, Yoichi; Yatsunami, J.; Hara, Nobuyuki

doi:10.1038/sj.gt.3300608

Cited by 52 publications

(30 citation statements)

References 18 publications

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“…We have previously shown that H157 cells, which have a mutated p53 gene, undergo apoptosis when infected with Ad5p53. 23 Ad5p53 infection of H157 cells at MOI 0.1 showed a weak cytotoxic effect compared with Ad5VEGFE1. Similar results were obtained with A427 cells (data not shown).…”

Section: Specific Cell Killing Efficacy Of Vegf Promoter Driving Cradmentioning

confidence: 88%

“…We also used wild-type Ad5 (Ad5wt) as a control. 23 The viruses were propagated in the Ad packaging cell line, 293HEK, and purified by double cesium chloride density gradient centrifugation, followed by dialysis against phosphate-buffered saline with 10% glycerol. The viral particle (VP) concentration was determined spectrophotometrically, using a conversion factor of 1.1 Â 10 12 VPs per absorbance unit at 260 nm, 24 and standard plaque assays on 293 cells were performed to determine infectious particles.…”

Section: Adenovirus Vectorsmentioning

confidence: 99%

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Vascular endothelial growth factor promoter-based conditionally replicative adenoviruses for pan-carcinoma application

Takayama

Adachi

et al. 2006

Cancer Gene Ther

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Treatment of advanced lung cancer is one of the major challenges in current medicine because of the high morbidity and mortality of the disease. Advanced stage lung cancer is refractory to conventional therapies and has an extremely poor prognosis. Thus, new therapeutic approaches are needed. Lung tumor formation depends on angiogenesis in which the vascular endothelial growth factor (VEGF) produced by cancer cells plays a pivotal role. Neutralizing VEGF with a soluble VEGF receptor suppresses tumor growth; however, the anticancer effect with this therapy is weakened after the intratumoral vascular network is completed. In this study, we turned the expression of VEGF by tumors to therapeutic advantage using a conditionally replication-competent adenovirus (CRAd) in which the expression of E1 is controlled by the human VEGF promoter. This virus achieved good levels of viral replication in lung cancer cells and induced a substantial anticancer effect in vitro and in vivo. As a further enhancement, the cancer cell killing effect was improved with tropism modification of the virus to express the knob domain of Ad3, which improved infectivity for cancer cells. These VEGF promoter-based CRAds also showed a significant cell killing effect for various types of cancer lines other than lung cancer. Conversely, the VEGF promoter has low activity in normal tissues, and the CRAd caused no damage to normal bronchial epithelial cells. Since tumor-associated angiogenesis via VEGF signalling is common in many types of cancers, these CRAds may be applicable to a wide range of tumors. We concluded that VEGF promoter-based CRAds have the potential to be an effective strategy for cancer treatment.

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Section: Specific Cell Killing Efficacy Of Vegf Promoter Driving Cradmentioning

confidence: 88%

Section: Adenovirus Vectorsmentioning

confidence: 99%

Vascular endothelial growth factor promoter-based conditionally replicative adenoviruses for pan-carcinoma application

Takayama

Adachi

et al. 2006

Cancer Gene Ther

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“…This variability could be at least partially attributed to the variability in CAR and integrin expression levels that are required for viral uptake into the cells. [76][77][78][79][80][81][82][83][84] To demonstrate suppression of cell growth in the sarcoma cell lines, lower doses of Ad-wtp53 were used so as not to produce an overt cytotoxic effect with massive cell death as seen in our previous experiments. Doses ranging from 0.1 to 0.4 PFU/cell (2-10 PFU/cell for RD) were used and a cell count was performed every 24 hours for 5 days.…”

Section: Discussionmentioning

confidence: 99%

Adenovirus-mediated p53 gene therapy in pediatric soft-tissue sarcoma cell lines: sensitization to cisplatin and doxorubicin

et al. 2004

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Sarcomas, or tumors of connective tissue, represent roughly 20% of childhood cancers. Although the cure rate for sarcomas in general has significantly improved in the last 10 years, there continue to be subgroups that are difficult to treat. High-grade or metastatic soft-tissue sarcomas and rhabdomyosarcomas (RMS) of the extremities remain therapeutic challenges and their prognosis is often poor. The future of sarcoma therapy will likely include molecular approaches including gene/protein expression profiling and gene-based therapy. Most sarcomas harbor defects in the p53 or pRb pathways. The tumor suppressor p53 is central to regulation of cell growth and tumor suppression and restoring wild-type p53 function in pediatric sarcomas may be of therapeutic benefit. Studies with adenoviral-mediated p53 gene transfer have been conducted in many cancer types including cervical, ovarian, prostatic and head and neck tumors. Studies of this approach, however, remain limited in pediatric cancers, including sarcomas. Using three viral constructs containing cDNA for wild-type p53, mutant p53 (C135S) and lacZ, we studied the effect of adenoviralmediated gene therapy in four pediatric sarcoma cell lines, RD and Rh4 (RMS), Rh1 (Ewing's sarcoma) and A204 (undifferentiated sarcoma). Using the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay, we have shown a dose-dependent decrease in cell viability 72 h post-treatment that occurs with Ad-wtp53 but not with Ad-mutp53. Cells treated with Ad-wtp53 show upregulation of the p53 downstream targets, p21 CIP1/WAF1 and bax. Growth curves demonstrate suppression of cell growth over a period of 4 days and cells treated with Ad-wtp53 demonstrate a significant increase in sensitivity to the chemotherapeutic agents, cisplatin and doxorubicin. Our results indicate that restoration of wild-type p53 function in pediatric sarcoma cells could provide a basis for novel approaches to treatment of this disease.

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“…The p53 gene of NCI-H157 is mutated (exon 8, codon 298, CAG to TAG) 4 and that of NCI-H1299 is deleted, and both cell lines exhibited a high gene transfer effect when cultured with adenoviral vectors. 5 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide (XTT) was purchased from Sigma (St Louis, Mo). The anticancer agents used included CDDP, carboplatin (CBDCA), and paclitaxel (all from Bristol-Myers Squibb, Tokyo, Japan); 7-ethyl-10-hydroxy-camptothecin (SN-38) (from Yakult Honsha, Tokyo, Japan); bleomycin (BLM) and VP-16 (from Nippon Kayaku, Tokyo, Japan); 5-FU and adriamycin (ADR) (from Kyowa Hakko Kogyo, Tokyo, Japan); cyclophosphamide (CPM), vindesin (VDS), and ifosfamide (IFO) (from Shionogi and Co., Osaka, Japan); and SM-5887-13-OH (an active metabolite of newly developed anthracyclin) (from Sumitomo Pharmaceuticals, Osaka, Japan).…”

Section: Cell Culture and Chemicalsmentioning

confidence: 99%

“…Replication-defective E1 and E3 adenoviral vectors expressing human wt p53 5,6 were prepared as described previously. 7 A cDNA coding for human wt p53 (kindly provided by Dr. Vogelstein, Program in Human Genetics, Johns Hopkins Oncology Center, Baltimore, Md) was placed into a cassette cosmid vector, pAdexCA1w (provided by Dr. Saito, University of Tokyo, Tokyo, Japan), under a CA promoter comprising a cytomegalovirus enhancer and chicken ␤-actin promoter (pAdex1w/p53).…”

Section: Adenoviral Vectormentioning

confidence: 99%

Alteration of drug chemosensitivity caused by the adenovirus-mediated transfer of the wild-type p53 gene in human lung cancer cells

Osaki¹,

Nakanishi²,

Takayama³

et al. 2000

Cancer Gene Ther

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The aim of the present study is to identify the optimal anticancer agents for use in combination with gene therapy using wild-type (wt) p53 gene transfer. We used adenoviral vectors expressing human wt p53 (AdCAp53) and investigated the effects of wt p53 gene transfer in combination with 12 anticancer agents on a human pulmonary squamous cell carcinoma cell line, NCI-H157, and a human pulmonary large cell carcinoma cell line, NCI-H1299. Solutions containing anticancer agents at various concentrations were added followed by the addition of recombinant adenovirus solutions; after a 5-day incubation period, the anticancer activity was then evaluated by a 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide assay. Each 50% inhibitory concentration was calculated based on the dose-response curves. The agents showing a high degree of effectiveness on NCI-H157 cells were cisplatin (CDDP), 5-fluorouracil (5-FU), bleomycin, and 7-ethyl-10-hydroxy-camptothecin (SN-38), an active metabolite of irinotecan (CPT-11); conversely, cyclophosphamide and paclitaxel showed a low degree of effectiveness. Based on these data, an isobologram was performed to investigate the interaction between AdCAp53 and some anticancer agents. A supra-additive effect was thus observed for 5-FU and SN-38 on NCI-H157 cells. An additive effect was also observed for CDDP, paclitaxel, bleomycin, and cyclophosphamide on NCI-H157 cells. CDDP, paclitaxel, 5-FU, and SN-38 had an additive effect on NCI-H1299 cells. No drug showed any subadditive or protective effects. These findings suggest that CPT-11 and 5-FU may thus be useful as possible anticancer agents for use in a combination therapy regimen using wt p53 gene transfer. CDDP and CPT-11 had a significant antitumoral effect on H157 cell xenografts of nude mice in vivo. These results indicate that CPT-11 as well as CDDP would be a candidate for the combination of chemotherapy and gene therapy for non-small cell lung cancer. Cancer Gene Therapy (2000) 7, 300 -307

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The levels of integrin αvβ5 may predict the susceptibility to adenovirus-mediated gene transfer in human lung cancer cells

Cited by 52 publications

References 18 publications

Vascular endothelial growth factor promoter-based conditionally replicative adenoviruses for pan-carcinoma application

Vascular endothelial growth factor promoter-based conditionally replicative adenoviruses for pan-carcinoma application

Adenovirus-mediated p53 gene therapy in pediatric soft-tissue sarcoma cell lines: sensitization to cisplatin and doxorubicin

Alteration of drug chemosensitivity caused by the adenovirus-mediated transfer of the wild-type p53 gene in human lung cancer cells

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