Radiation-inducible silencing of uPA and uPAR in vitro and in vivo in meningioma

Rao, Rajesh P. N.

doi:10.3892/ijo_00000557

Cited by 7 publications

(3 citation statements)

References 35 publications

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“…After transfection for 24 h, the transfected cells were irradiated by linear accelerator (Primvs, Siemens, Germany) at a dose of 3 Gy. We chose the radiation dose of 3 Gy based on our previous research [8]. The monolayers of the transfected cells in the control group were also mock-irradiated and subse quently treated identically as with the irradiated monolayers of transfected cells.…”

Section: The Killing Effect Of Puma Gene Mediated By Radiation-inducimentioning

confidence: 99%

“…Tca8113 cells were transfected with Lipofectamine (GIBCO) by modifying the manufacturer's procedure based on our previous study [7,8]. Tca8113 cells (2 × 10 5 ) were seeded into a six-well plate at 2 × 10 5 cells per well, and conventionally maintained for 24 h. A total of 24 wells of Tca8113 cells were prepared to be transfected.…”

Section: The Killing Effect Of Puma Gene Mediated By Radiation-inducimentioning

confidence: 99%

“…Although its specific mechanism for inducing apoptosis needs further explanation, the proapoptotic function has achieved rather good results, becoming a promising new target in gene therapy [4][5][6]. Radiation-inducible promoters can regulate and control the downstream therapeutic gene expression, a new strategy for radiation-gene therapy founded in recent years [7,8]. It combines traditional radiation treatment with gene therapy, which may reduce radiation dosage and increases efficacy of gene therapy [9,10].…”

Section: Introductionmentioning

confidence: 99%

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Radiation-inducible promoter mediated PUMA Gene in the the treatment of Tca8113

Yu¹,

Zhao²,

Luo³

et al. 2011

OJST

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Objective: The aim of this study is to explore the therapeutic effect of the PUMA gene mediated by radiation-inducible promoters in the treatment of tongue squamous cell carcinoma. Methods: Recombinant pcDNA3.1 (+)/E-PUMA was constructed, in which the PUMA gene was mediated by a synthetic radiation inducible promoter. The recombined plasmids were transfected into the Tca8113 cell and xenografts of human tongue squamous carcinoma in naked mice respectively. After 24 h, the tumors were treated with 3 Gy of irradiation to upregulate the PU-MA gene expression. PUMA mRNA was detected by RT-PCR. Proliferating cell nuclear antigen (PCNA) and apoptosis were detected by immunohistochemical method and in situ end-labeling (ISEL) respectively. The data were analyzed using the SPSS11.0 software package for chi-square test. Results: Compared with the control group, the comparative survival rate of Tca8113 cells in the PUMA/IR group was markedly decreased and the xenografts were signifycantly suppressed. Up-regulation of PUMA gene expression was observed in the Tca8113 cells and in the xenografts after irradiation. The apoptosis indices of the Tca-8113 cells and xenograft with irradiation were markedly higher than those without irradiation. At the same time, the proliferation indices of the Tca8113 cells and xenografts with irradiation were markedly lower than those without irradiation. Conclusions: radiation-inducible promoters can serve as molecular switches to improve the expression of PUMA gene in tongue squamous cell carcinoma both in vivo and in vitro. Low-dose induction radiation can significantly improve therapeutic efficiency.

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Section: The Killing Effect Of Puma Gene Mediated By Radiation-inducimentioning

confidence: 99%

Section: The Killing Effect Of Puma Gene Mediated By Radiation-inducimentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Radiation-inducible promoter mediated PUMA Gene in the the treatment of Tca8113

Yu¹,

Zhao²,

Luo³

et al. 2011

OJST

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Multiple uses of basement membrane‐like matrix (BME/Matrigel) in vitro and in vivo with cancer cells

Benton

Kleinman

George

et al. 2011

Intl Journal of Cancer

188

134

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Significant advances in our understanding of cancer cell behavior, growth, and metastasis have been facilitated by studies using a basement membrane-like extracellular matrix extract, also known as Matrigel. The basement membrane is a thin extracellular matrix that is found in normal tissues and contacts epithelial and endothelial cells, smooth muscle, fat, Schwann cells, etc. It is composed of mainly laminin-111, collagen IV, heparan sulfate proteoglycan, entactin/nidogen, and various growth factors (fibroblast growth factor, transforming growth factor beta, epidermal growth factor, etc.). Most tumors of epithelial origin produce significant amounts of basement membrane matrix and interact with it particularly during metastasis. Cancer cells metastasize via degradation of the vessel basement membrane matrix to extravasate into the blood stream and colonize distant sites. This review will focus on the interaction of cancer cells and cancer stem cells with the basement membrane-like matrix and the various uses of this interaction to accelerate tumor growth in vivo and to develop in vitro assays for invasion, morphology, and dormancy. Such assays and methods have advanced our understanding of the process of cancer progression, the genes and pathways that are involved, the potential of various therapeutic agents, the effects of neighboring cells, and the role of stem cells.

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Mebendazole and radiation in combination increase survival through anticancer mechanisms in an intracranial rodent model of malignant meningioma

2018

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Purpose Meningiomas are a frequent tumor of the central nervous system. Although mostly benign, approximately 5% present as atypical or malignant tumors. Treatments for atypical meningiomas include gross total resection and radiotherapy, but about 33% of patients have recurrent tumors, sometimes as a higher grade. Recently, the brain penetrant anthelmintic drug, mebendazole, has shown promise as an anticancer agent in rodent models of glioblastoma and medulloblastoma. Methods The half maximal inhibitory concentration (IC50), effect on; colony formation, cell proliferation, and caspase-3/7 markers of apoptosis of mebendazole with and without radiation was measured in vitro. Mice intracranially implanted with KT21MG1 human meningioma were administered mebendazole alone or in combination with radiation. Survival benefit was evaluated, while tumors were investigated by immunohistochemical staining for apoptosis, cell proliferation, and vascular density. Results In vitro experiments on meningioma cell lines showed the IC50 for mebendazole in the range of 0.26 to 0.42 μM. Mebendazole alone induced cytotoxicity, however the combination had a greater reduction in colony formation and resulted in higher levels of cleaved caspase-3. The in vivo study showed both, mebendazole alone and the combination, to have a survival benefit with an increase in apoptosis, and decreases in tumor cell and vascular proliferation. Conclusion These preclinical findings indicate that mebendazole alone or in combination with radiation can be considered for the treatment of malignant meningioma. The mechanism of action for this combination may include an increase in apoptosis, a reduction in proliferation and angiogenesis, or a combination of these effects.

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Radiation-inducible silencing of uPA and uPAR in vitro and in vivo in meningioma

Cited by 7 publications

References 35 publications

Radiation-inducible promoter mediated PUMA Gene in the the treatment of Tca8113

Radiation-inducible promoter mediated PUMA Gene in the the treatment of Tca8113

Multiple uses of basement membrane‐like matrix (BME/Matrigel) in vitro and in vivo with cancer cells

Mebendazole and radiation in combination increase survival through anticancer mechanisms in an intracranial rodent model of malignant meningioma

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