Re: MicroRNA Regulation of Oncolytic Herpes Simplex Virus-1 for Selective Killing of Prostate Cancer Cells

Re: MicroRNA Regulation of Oncolytic Herpes Simplex Virus-1 for Selective Killing of Prostate Cancer Cells

Re: MicroRNA Regulation of Oncolytic Herpes Simplex Virus-1 for Selective Killing of Prostate Cancer Cells
Oncolytic viruses could turn out to be the most important advance in cancer treatment for 30 years. (2006). Cancer virotherapy functions by converting the natural cell killing ability of a benign virus to selectively kill cancer cells. Research thus far shows that the presence of a functional anti-tumor T cell response directly correlates with positive cancer outcomes [3,4]. Cells were maintained in Dulbecco’s modified Eagle’s medium supplemented with 10% fetal bovine serum, 2 mM L-glutamine, 100 U ml−1 of penicillin and streptomycin at 37 °C under 5% CO2. Our results support the concept that augmentation of the anti-IFN strategies of HSV, using a molecule from a different virus, can potentiate the oncolytic effect of the therapeutic virus. Oncolytic virotherapy is a promising anticancer therapy because efficient transduction and cancer cell-specific viral replication can boost therapeutic efficacy.3, 4, 5, 6, 7 Therefore, oncolytic viral therapy is viewed as a new strategy for the treatment of advanced cancers.

Assays with chimeric tumor mixtures of TK+/TK− cells showed that the level of the bystander killing obtained was characteristic of the TK− bystander cells. HSV-TK/GCV as part of a multitargeted approach has produced more promising results in prostate cancer19,20. 20–30 l to achieve 100 mg/kg). An attractive option for clinical use is a highly proliferative subpopulation of bone marrow–derived MSCs called bone marrow–derived multipotent adult progenitor cells (MAPCs), which can be expanded for more than 100 PDs without exogenous immortalization. This approach is simple and practical from an experimental point of view however perhaps less pragmatic in a clinical setting. We tested in vivo effects of the mutant in a metastatic breast cancer mouse model after introducing it into NSCs by baculoviral transduction and injecting the transduced NSCs via tail vein into mice. Additionally, estrogenic effects on cells have been demonstrated to decrease the efficacy of various chemotherapeutics and radiation therapy in vitro(3–6).

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