Advances in Viral Vector-Based TRAIL Gene Therapy for Cancer

Norian, Lyse A.; James, Britnie R.; Griffith, Thomas S.

doi:10.3390/cancers3010603

Cited by 14 publications

(13 citation statements)

References 103 publications

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“…TRAIL binds to its specific receptors TRAILR1 (death receptor 4) and TRAILR2 (death receptor 5), causing activation of the death domain and cell apoptosis. 72,73 In addition, TRAIL has also been found to bind with TRAILR3 (TRID/ DcR1) and TRAILR4 (DcR2) decoy receptors, which do not contain any cytoplasmic death domain and thus cannot induce cell apoptosis. Therefore, binding TRAIL to these receptors acts as an antagonist, because it will not activate any cell-death signaling.…”

Section: Tumor-necrosis Factor-αmentioning

confidence: 99%

“…Caspase activation leads to the cleavage of target proteins responsible for preserving cellular function, resulting in cell apoptosis. 73,74 The use of TRAIL as an agent to kill cancer cells arises from its preferential ability to induce cell apoptosis in cancer cells without harming normal healthy cells. 75,76 Ashkenazi et al 72 examined the apoptotic effect of TRAIL in various normal and cancerous cells.…”

Section: Tumor-necrosis Factor-αmentioning

confidence: 99%

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Targeted nonviral gene therapy in prostate cancer

Altwaijry¹,

Somani²,

Dufès³

2018

IJN

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Prostate cancer is the second-most widespread cancer in men worldwide. Treatment choices are limited to prostatectomy, hormonal therapy, and radiotherapy, which commonly have deleterious side effects and vary in their efficacy, depending on the stage of the disease. Among novel experimental strategies, gene therapy holds great promise for the treatment of prostate cancer. However, its use is currently limited by the lack of delivery systems able to selectively deliver the therapeutic genes to the tumors after intravenous administration without major drawbacks. To remediate this problem, a wide range of nonviral delivery approaches have been developed to specifically deliver DNA-based therapeutic agents to their site of action. This review provides an overview of the various nonviral delivery strategies and gene therapy concepts used to deliver therapeutic DNA to prostate cancer cells, and focuses on recent therapeutic advances made so far.

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Section: Tumor-necrosis Factor-αmentioning

confidence: 99%

Section: Tumor-necrosis Factor-αmentioning

confidence: 99%

Targeted nonviral gene therapy in prostate cancer

Altwaijry¹,

Somani²,

Dufès³

2018

IJN

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“…Treatments against all types of cancer aim to interfere the functioning of transformed cells. Traditionally, this interference was induced by using drugs that block the cell growth together with radiotherapy [95,96]. This approach has been the most successful; however, produces serious collateral effects on patients.…”

Section: Therapeutics Approaches Against Cancermentioning

confidence: 99%

“…Another novel approach to treat cancer is gene therapy, which uses many genes to alter the functioning of transformed cells blocking survival mechanisms and triggering apoptosis [1,96,104]. Other original strategies related with gene therapy use micro-RNA specifically designed to avoid the overexpression of oncogenes like BCL2 family or p53 in cancerous cells [105,106].…”

Section: Therapeutics Approaches Against Cancermentioning

confidence: 99%

Dynamics of p53 and Cancer

Bensussen¹,

Dı́az²

2015

Evolution of Ionizing Radiation Research

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Cancer is a multifactorial disease in which cell types lost their capability to regulate growth, proliferation, and cell death pathways, causing the uncontrolled proliferation of tumor cells. Cell death pathway is supported by the operation of the p53-Mdm2negative feedback loop that has a central role to prevent the development of tumor cells. Under severe DNA damage, this loop takes the control of the apoptotic pathway and activates Bax, which, in turn, activates the caspase cascade to produce the death of the injured cell. However, events like Mdm2 overexpression or the suppression of caspase-9 gene can block the transmission of the death signal to the caspase cascade allowing the survival of the mutated cell. In this chapter, a mathematical model that explores the effect of Mdm2 overexpression and the suppression of caspase-9 on the control of death by the p53-Mdm2 loop is presented. From the model, two strategies for tumor cell survival are indentified, showing how mutations that affect the death pathway allow the survival of transformed cells. The model suggests that the combination of different simultaneous treatments against these mutations can be a suitable strategy against cancer.

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“…20, 21 The TRAIL protein belongs to the TNF cytokine superfamily. After binding with death receptors (DR4 and DR5) and decoy receptors (DcR1 and DcR2), the extrinsic apoptotic pathway is triggered by TRAIL through recruitment of the Fas-associated death domain protein to the death domain.…”

Section: Introductionmentioning

confidence: 99%

PSMA-specific theranostic nanoplex for combination of TRAIL gene and 5-FC prodrug therapy of prostate cancer

et al. 2016

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Metastatic prostate cancer causes significant morbidity and mortality and there is a critical unmet need for effective treatments. We have developed a theranostic nanoplex platform for combined imaging and therapy of prostate cancer. Our prostate-specific membrane antigen (PSMA) targeted nanoplex is designed to deliver plasmid DNA encoding tumor necrosis factor related apoptosis-inducing ligand (TRAIL), together with bacterial cytosine deaminase (bCD) as a prodrug enzyme. Nanoplex specificity was tested using two variants of human PC3 prostate cancer cells in culture and in tumor xenografts, one with high PSMA expression and the other with negligible expression levels. The expression of EGFP-TRAIL was demonstrated by fluorescence optical imaging and real-time PCR. Noninvasive 19F MR spectroscopy detected the conversion of the nontoxic prodrug 5-fluorocytosine (5-FC) to cytotoxic 5-fluorouracil (5-FU) by bCD. The combination strategy of TRAIL gene and 5-FC/bCD therapy showed significant inhibition of the growth of prostate cancer cells and tumors. These data demonstrate that the PSMA-specific theranostic nanoplex can deliver gene therapy and prodrug enzyme therapy concurrently for precision medicine in metastatic prostate cancer.

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Advances in Viral Vector-Based TRAIL Gene Therapy for Cancer

Cited by 14 publications

References 103 publications

Targeted nonviral gene therapy in prostate cancer

Targeted nonviral gene therapy in prostate cancer

Dynamics of p53 and Cancer

PSMA-specific theranostic nanoplex for combination of TRAIL gene and 5-FC prodrug therapy of prostate cancer

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