TMZ, while the genetically modified oncolytic HSV has a decreased However, certain types of cancer cellsĪre able to repair TMZ-induced DNA damage, leading to resistance to Of DNA alkylation and methylation damage in cancer cells ( 12). In addition, TMZ has been used inĬlinical trials for the treatment of advanced metastatic melanoma Of malignant glioma because it is able to easily pass through theīlood-brain barrier due to its low molecular weight and Temozolomide (TMZ) is an imidazotetrazine-derivedĪlkylating agent used as a first-line oral drug for the treatment Glioblastoma in clinical trials in Japan ( 7). HSV-1 vector derived from G207 with the deletion of the infectedĬell protein 47 (ICP47) gene and both copies of the γ34.5 gene Oncolytic HSV G47Δ is a third-generation replication-competent Genetically modified herpes simplex virus (HSV), has been approvedīy the US Food and Drug Administration for clinical application in Oncolytic viruses have been geneticallyĮngineered to improve both the safety of treatment and selectivity ![]() Potential novel therapeutic strategy for cancer treatment ( 4). Oncolytic virus-based therapy has been regarded as a The host immune response in infected cancer cells, which resultsįrom cancer antigen exposure in lysed cancer cells ( 3). In, and kill cancer cells via induction of cancer cell lysis and Oncolytic viruses can selectively infect, replicate Need to develop new effective therapeutic approaches for breast Response to radiotherapy and drug resistance to chemotherapy Surgery to eliminate distant metastasis, the lack of durable Including surgery, radiotherapy and chemotherapy, can successfullyĬure patients or prolong patient survival in the majority of cases,Įach of these therapies has limitations, such as the inability of Synergy between G47Δ and TMZ was at least partially mediated via TMZ‑induced acceleration of G47Δ replication, and such a synergy in breast cancer cells in vitro and in vivo provides novel insight into the future development of a therapeutic strategy against breast cancer.īreast cancer is the most common life-threateningĬancer in women globally, with an annual rate of new cases reachingġ26/100,000 women and a death rate of ~30% ( 1). The combined administration of G47Δ and TMZ also effectively suppressed breast cancer cell‑derived tumor growth in vivo, compared with the administration of G47Δ or TMZ alone. G47Δ and TMZ served a synergistic role resulting in decreased breast cancer cell viability, induction of cell cycle arrest, promotion of tumor cell apoptosis and enhancement of DNA damage response in vitro. The role of G47Δ and TMZ in suppressing tumorigenesis in vivo was investigated in a xenograft mouse model. Cell viability, flow cytometry, reverse transcription quantitative‑PCR and western blotting were performed to investigate the synergy between G47Δ and TMZ in regulating breast cancer cell behavior in vitro. ![]() The human breast cancer cell lines SK‑BR‑3 and MDA‑MB‑468 were treated with G47Δ and TMZ individually or in combination. The objective of the present study was to investigate the role and underlying mechanism of G47Δ and TMZ, in combination, in breast cancer cell tumorigenesis. However, the combined effect of G47Δ and TMZ on cancer cells, particularly on breast cancer cells, remains largely unknown. The oncolytic herpes simplex virus (HSV) G47Δ can selectively eliminate glioblastoma cells via viral replication and temozolomide (TMZ) has been clinically used to treat glioblastoma.
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