Synergy of enediyne antibiotic lidamycin and temozolomide in suppressing glioma growth with potentiated apoptosis induction

Li, Xingqi; Ouyang, Zhi-Gang; Zhang, Shenghua; Liu, Hong; Shang, Yue; Li, Yang; Zhen, Yong‐Su

doi:10.1007/s11060-014-1477-3

Cited by 9 publications

(9 citation statements)

References 35 publications

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“…Temozolomide (TMZ) is the first agent in 20 years approved by the FDA to treat glioblastoma and has been one of the most commonly used anti-glioma agents with limited adverse effects [ 6 , 7 ] due to its ability penetrating the blood brain barrier (BBB). The standard treatment is maximal surgical resection and maintenance treatment with temozolomide (TMZ), which could improve median and 5-year survival significantly [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

The synergic antitumor effects of paclitaxel and temozolomide co-loaded in mPEG-PLGA nanoparticles on glioblastoma cells

Shen

et al. 2016

Oncotarget

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To get better chemotherapy efficacy, the optimal synergic effect of Paclitaxel (PTX) and Temozolomide (TMZ) on glioblastoma cells lines was investigated. A dual drug-loaded delivery system based on mPEG-PLGA nanoparticles (NPs) was developed to potentiate chemotherapy efficacy for glioblastoma. PTX/TMZ-NPs were prepared with double emulsification solvent evaporation method and exhibited a relatively uniform diameter of 206.3 ± 14.7 nm. The NPs showed sustained release character. Cytotoxicity assays showed the best synergistic effects were achieved when the weight ratios of PTX to TMZ were 1:5 and 1:100 on U87 and C6 cells, respectively. PTX/TMZ-NPs showed better inhibition effect to U87 and C6 cells than single drug NPs or free drugs mixture. PTX/TMZ-NPs (PTX: TMZ was 1:5(w/w)) significantly inhibited the tumor growth in the subcutaneous U87 mice model. These results indicate that coordinate administration of PTX and TMZ combined with NPs is an efficient method for glioblastoma.

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Section: Introductionmentioning

confidence: 99%

The synergic antitumor effects of paclitaxel and temozolomide co-loaded in mPEG-PLGA nanoparticles on glioblastoma cells

Shen

et al. 2016

Oncotarget

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“…For in vivo drug-combination analysis, we employed the fractional product method. 57,58 The efficacy of each monotherapy and the combination therapy were assessed as the fractional tumor volume (FTV). FTV was calculated based on the following equation: (the mean volume of the treated tumors)/(that of the control tumors).…”

Section: The Combination Therapymentioning

confidence: 99%

Oncolytic herpes virus G47Δ works synergistically with CTLA-4 inhibition via dynamic intratumoral immune modulation

Sugawara¹,

Iwai²,

Ito³

et al. 2021

Molecular Therapy - Oncolytics

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Oncolytic virus therapy can increase the immunogenicity of tumors and remodel the immunosuppressive tumor microenvironment, leading to an increased antitumor response to immune-checkpoint inhibitors. Here, we investigated the therapeutic potential of G47D, a third-generation oncolytic herpes simplex virus type 1, in combination with immune-checkpoint inhibitors using various syngeneic murine subcutaneous tumor models. Intratumoral inoculations with G47D and systemic anti-cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) antibody administration caused an enhanced antitumor activity when combined and worked synergistically. Conversely, the efficacy of G47D in combination with anti-programmed cell death protein-1 (PD-1) antibody was equivalent to that of the anti-PD-1 antibody alone in all murine models examined. The combination of intratumoral G47D and systemic anti-CTLA-4 antibody was shown to recruit effector T cells into the tumor efficiently while decreasing regulatory T cells. Furthermore, a wide range of gene signatures related to inflammation, lymphoid lineage, and T cell activation was highly upregulated with the combination therapy, suggesting the conversion of immune-insusceptible tumors to immune susceptible. The therapeutic effect proved tumor specific and long lasting. Immune cell subset depletion studies demonstrated that CD4 + T cells were required for synergistic curative activity. The results depict the dynamics of immune modulation of the tumor microenvironment and provide a clinical rationale for using G47D with immune checkpoint inhibitors.

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“…Multiple targets for the emergence of drug-resistant tumors should aim to reduce the toxicity of chemotherapy and improve its efficacy (28). Research conducted on the synergistic properties of antitumor drugs gain attention so as to regulate apoptotic pathways, reverse multidrug resistance, inhibit tumor migration and invasion, and prevent angiogenesis system (3,6,14). In patient with GBM is resistant to some chemotherapeutic drugs because of the MGMT gene in glioma cells (23), which is highly expressed in solid types of cancer, resulting in the removal of the druginduced cytotoxic O6-alkylguanine DNA adducts.…”

Section: Ea Combined With Tmz Failed To Downregulate Mdr1 Expression (Abcb1)mentioning

confidence: 99%

Ellagic acid enhances antitumor efficacy of temozolomide in an in vitro glioblastoma model

Çetin

Biltekin²

2019

Turkish Neurosurgery

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To observe the effect of combining ellagic acid (EA), a natural phenol present in fruits and vegetables, and temozolomide (TMZ) on the proliferation and expression profile of C6 glioma cell line.MATERIAL and METHODS: Rat C6 glioma cells were treated with 100-µM EA combined with 100 µM TMZ for 24, 48, and 72 hours (h). Cell proliferation and p53 and caspase-3 protein levels were evaluated using immunocytochemistry. Multi drug resistance 1 (MDR1), O6-methylguanine-DNA methyltransferase (MGMT), and apoptotic protein (caspase-3 and p53) expressions were assessed using reverse transcription polymerase chain reaction (RT-PCR).RESULTS: EA combined with TMZ conspicuously reduced the cell viability at all incubation times (p<0.001). EA significantly downregulated MGMT expression regardless of the presence of TMZ even at early hours (p<0.001). The combination therapy reduced MDR1 expression only on 48 h in comparison with TMZ alone. EA alone upregulated caspase-3 at 48 h but upregulated p53 at 48 and 72 h. The combined therapy enhanced the immunoreactivities of p53 and caspase-3 proteins independent of the treatment durations but not of the genes.CONCLUSION: EA combined with TMZ may have a potential antiproliferative efficacy by inhibiting MGMT expression and activating apoptotic protein, p53 and caspase-3, expression.

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Synergy of enediyne antibiotic lidamycin and temozolomide in suppressing glioma growth with potentiated apoptosis induction

Cited by 9 publications

References 35 publications

The synergic antitumor effects of paclitaxel and temozolomide co-loaded in mPEG-PLGA nanoparticles on glioblastoma cells

The synergic antitumor effects of paclitaxel and temozolomide co-loaded in mPEG-PLGA nanoparticles on glioblastoma cells

Oncolytic herpes virus G47Δ works synergistically with CTLA-4 inhibition via dynamic intratumoral immune modulation

Ellagic acid enhances antitumor efficacy of temozolomide in an in vitro glioblastoma model

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