702 Quantitative analysis of p53-targeted gene expression and visualization of p53 transcriptional activity following intratumoral administration of adenoviral p53 in vivo

Ohtani, Shoichiro; Kagawa, Shunsuke; Tsunemitsu, Yousuke; Tokunaga, Naoko; Roth, Joachim; Tanaka, Nobushige; Fujiwara, T.

doi:10.1016/s1359-6349(03)90733-6

Cited by 13 publications

(14 citation statements)

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“…Among these genes, MDM2 and BIRC5 were known to be involved in cell proliferation and anti-apoptosis. 16,17,21 In addition, among these two genes, only MDM2 was significantly promoted by aldosterone compared with control in a RT/real-time PCR study ( Table 2). Therefore we further examined the features of MDM2 as an aldosterone-responsive gene in HASMC and whether MDM2 was associated with aldosterone-induced promotion of MR-positive VSMC proliferation using further quantitative RT/real-time PCR, immunoblotting analysis, immunoflourescence analysis, and siRNA transfection assay described above.…”

Section: Mr Expression In Hasmcmentioning

confidence: 98%

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MDM2: A Novel Mineralocorticoid-Responsive Gene Involved in Aldosterone-Induced Human Vascular Structural Remodeling

Nakamura

Suzuki

et al. 2006

The American Journal of Pathology

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Aldosterone has been demonstrated to play an important role in the pathogenesis of various cardiovascular diseases. Vascular structural remodeling, including vascular smooth muscle cell (VSMC) proliferation, has been also reported in small resistance arteries of patients with primary aldosteronism. Therefore, in this study, we examined whether genes involved in the regulation of the cell cycle were induced by aldosterone alone in cultured human VSMCs and in human small resistance arteries. Results of these studies eventually demonstrated that MDM2, one of the genes involved in anti-apoptosis and cell growth, was markedly increased in mineralocorticoid receptor ( Aldosterone is a steroid hormone synthesized in the zona glomerulosa of human adrenal cortex as a result of stimulation by angiotensin II and others.

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Section: Mr Expression In Hasmcmentioning

confidence: 98%

“…The information of primers used in this study is summarized in Table 1. 16,17 We independently triplicated the same experiments for confirmation.…”

Section: Gene Chip Microarray Assay and Real-time Pcr Studymentioning

confidence: 99%

MDM2: A Novel Mineralocorticoid-Responsive Gene Involved in Aldosterone-Induced Human Vascular Structural Remodeling

Nakamura

Suzuki

et al. 2006

The American Journal of Pathology

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“…22,23 Second, the specific tumor cell killing does not rely on E1 mutations that can compromise the production yield, viral replication and spread. 24,25 Third, in contrast to the tumorspecific promoters, the systems utilize a more universal strong CMV promoter to achieve high transgene expression. Moreover, the transgene expression occurs in the late of Ad life cycle.…”

Section: Construction Of Hravs and Ehravsmentioning

confidence: 99%

Homologous recombination-based adenovirus vector system for tumor cell-specific gene delivery

Lü

Liu

et al. 2013

Cancer Biology & Therapy

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“…Replication-deficient adenoviral vectors containing human wild-type p53 cDNA (Ad-p53) and β-galactosidase cDNA (Ad-lacZ) were also used (23). These viruses were purified by CsCl 2 step gradient ultracentrifugation followed by CsCl 2 linear gradient ultracentrifugation, and their titers were determined by plaque assay in the 293 cells.…”

Section: Recombinant Adenovirusesmentioning

confidence: 99%

Preclinical Evaluation of Differentially Targeting Dual Virotherapy for Human Solid Cancer

Sakai

Kagawa

Yamasaki

et al. 2010

Molecular Cancer Therapeutics

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Multimodal approaches combining drugs that differentially function is the most popular regimen for treating human cancer. Understanding the molecular mechanisms underlying the synergistic, potentiative, and antagonistic effects of drug combinations could facilitate the discovery of novel efficacious combinations. We previously showed that telomerase-specific replication-competent adenovirus (Telomelysin,, in which the human telomerase reverse transcriptase promoter controls the adenoviral E1 gene expression, induces a selective antitumor effect in human cancer cells. Here, using E1-deleted replicationdeficient adenovirus expressing the p53 tumor suppressor gene (Advexin, Ad-p53) and OBP-301, we investigate how these adenoviruses that kill tumor cells with different mechanisms could work in combination on human cancer. We found that E1-deficient Ad-p53 could kill cancer cells more efficiently in the presence of OBP-301 than Ad-p53 alone or OBP-301 alone, because Ad-p53 could become replication-competent by being supplied adenoviral E1 from coinfected OBP-301 in trans. Ad-p53 plus OBP-301 induced high levels of p53 protein expression without p21 induction, resulting in apoptotic cell death documented by active caspase-3 expression with a cytometric bead array and an increased subdiploid apoptotic fraction of the cell cycle. For in vivo evaluation, nude mice xenografted with human lung tumors received intratumoral injection of OBP-301 and/or Ad-p53. Analysis of the growth of implanted tumors showed an enhanced antitumor effect in combination therapy. Our data show that Ad-p53 in combination with OBP-301 induces not only oncolytic but also apoptotic cancer cell death and enhances antitumor activity in vitro and in vivo, providing potential merits as a multimodal treatment for human cancer.

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702 Quantitative analysis of p53-targeted gene expression and visualization of p53 transcriptional activity following intratumoral administration of adenoviral p53 in vivo

Cited by 13 publications

References 0 publications

MDM2: A Novel Mineralocorticoid-Responsive Gene Involved in Aldosterone-Induced Human Vascular Structural Remodeling

MDM2: A Novel Mineralocorticoid-Responsive Gene Involved in Aldosterone-Induced Human Vascular Structural Remodeling

Homologous recombination-based adenovirus vector system for tumor cell-specific gene delivery

Preclinical Evaluation of Differentially Targeting Dual Virotherapy for Human Solid Cancer

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