Targeting of EGFR increase anti-cancer effects of arsenic trioxide: Promising treatment for glioblastoma multiform

Mesbahi, Yashar; Zekri, Ali; Ahmadian, Shahin; Ghavamzadeh, Ardeshir; Ghaffari, Seyed H.

doi:10.1016/j.ejphar.2017.12.041

Cited by 18 publications

(8 citation statements)

References 62 publications

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“…Over activation of this pathway may be directly related to resistance to arsenic trioxide as a drug. When erlotinib, an inhibitor of EGFR, was used in combination with arsenic trioxide, ROS levels increased and there were significant synergistic effects on survival, proliferation and migration as well as on the cell cycle [ 68 ]. The activation of downstream products of EGFR is related to the regulation of c-Myc.…”

Section: Enhanced Anti-glioma Effect Of Arsenic Trioxide Combined Witmentioning

confidence: 99%

Arsenic trioxide as a novel anti-glioma drug: a review

Fang

Zhang

2020

Cell Mol Biol Lett

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Arsenic trioxide has shown a strong anti-tumor effect with little toxicity when used in the treatment of acute promyelocytic leukemia (APL). An effect on glioma has also been shown. Its mechanisms include regulation of apoptosis and autophagy; promotion of the intracellular production of reactive oxygen species, causing oxidative damage; and inhibition of tumor stem cells. However, glioma cells and tissues from other sources show different responses to arsenic trioxide. Researchers are working to enhance its efficacy in anti-glioma treatments and reducing any adverse reactions. Here, we review recent research on the efficacy and mechanisms of action of arsenic trioxide in the treatment of gliomas to provide guidance for future studies.

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Section: Enhanced Anti-glioma Effect Of Arsenic Trioxide Combined Witmentioning

confidence: 99%

Arsenic trioxide as a novel anti-glioma drug: a review

Fang

Zhang

2020

Cell Mol Biol Lett

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“…Our results showed the combination of two ATO and Erlo drugs has a synergistic effect. In the study of Ghanbari et al 51 this synergistic effect was confirmed in terms of the presence of ATO reduces the resistance of cancer cells to Erlo 51 Mesbahi et al 52 showed that a combination of Erlo and ATO causes cell cycle arrest in the G2/M2 phase and changes in the expression of genes involved in cell cycle arrest (C5NB1, p53, and p21 genes). The expression of the p53 and p21 genes rises threefold to fourfold, whereas the CCNB1 gene, which is important for cell transition to G2/M phase, declines.…”

Section: Discussionmentioning

confidence: 88%

“…In this investigation, it was also shown that when the two medicines were combined, the amount of reactive oxygen species produced was about twice when compared with ATO. 52 In recent years, targeted and ligand-modified liposomes have gotten a lot of interest. In order to treat solid tumors, liposomes modified with RGD peptide were produced as a novel formulation for targeted administration with high loading efficiency and preserve releasing property.…”

Section: Discussionmentioning

confidence: 99%

Arsenic trioxide and Erlotinib loaded in RGD‐modified nanoliposomes for targeted combination delivery to PC3 and PANC‐1 cell lines

Khosravani

Mir

Mirzaei

et al. 2022

Biotech and App Biochem

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During the past few years, advances in drag delivery have provided many opportunities in the treatment of various diseases and cancer. Arsenic trioxide (ATO) and Erlotinib (Erlo) are two drugs, approved by the United States Food and Drug Administration to treat cancer, but their use is limited in terms of the toxicity of ATO and the low solubility of Erlo. This study aimed to prepare arginine‐glycine‐aspartic acid (RGD)‐decorated nanoliposomes (NLPs) containing Erlo and ATO (NLPs–ATO–Erlo–RGD) to increase the solubility and reduce the toxicity of Erlo and ATO for cancer treatment. The results of transmission electron microscopy and dynamic light scattering showed that NLPs were synthesized uniformly, with spherical shape morphology and particle sizes between 140 and 160 nm. High‐performance liquid chromatography and ICP–MS results showed that about 90% of the drug was loaded in the NLPs. In comparison with NLPs–ATO–Erlo, NLPs–ATO–Erlo–RGD demonstrated considerable toxicity against the αvβ3 overexpressing PC3 cell line in the MTT experiment. It had no effect on the PANC‐1 cell line. In addition, apoptosis assays using Annexin V/PI demonstrated that NLPs–ATO–Erlo–RGD generated the highest apoptotic rates in PC3 cells when compared with NLPs–ATO–Erlo and the combination of free ATO and Erlo. Furthermore, treatment with NLPs–ATO–Erlo–RGD in (p < 0.05) PC3 cell line significantly reduced EGFR level. It is concluded NLPs–ATO–Erlo–RGD as a novel drug delivery system may be a promising platform for the treatment of cancer.

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“…For instance, we have previously indicated that telomerase inhibition using BIBR1532 sensitizes breast cancer cells to low concentrations of ATO (24). In the case of GBM, erlotinib, an inhibitor of epidermal growth factor receptor (EGFR), has been found to enhance the cytotoxic effects of ATO (25). These findings suggest that using ATO in combination therapy with small molecule inhibitors is a promising strategy for treating GBM.…”

Section: Discussionmentioning

confidence: 99%

Blockade of Nuclear Factor-Κb (NF-Κb) Pathway Using Bay 11-7082 Enhances Arsenic Trioxide-Induced Antiproliferative Activity in U87 Glioblastoma Cells

et al. 2022

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Background: Glioblastoma (GBM), the most aggressive and common form of glioma, accounts for over 13,000 death per year in the United States which indicates the importance of developing novel strategies for the treatment of this fatal malignancy. Although Arsenic trioxide (ATO) hinders the growth and survival of GBM cells, the requirement of concentrations higher than 4 µM for triggering apoptotic cell death has questioned its safety profile. Since the NF-κB signaling pathway plays a crucial role in tumorigenesis and chemo-resistance, targeting this oncogenic pathway may sensitize GBM cells to lower concentrations of ATO. Methods: Anti-tumor effects of ATO as monotherapy and in combination with Bay 11-7082 were determined using MTT, crystal violet staining, Annexin V/PI staining and scratch assays. Quantitative reverse transcription-PCR (qRT-PCR) analysis was applied to elucidate the molecular mechanisms underlying the anti-tumor activity of this combination therapy. Results: Our results revealed that ATO and Bay 11-7082 synergistically inhibited the proliferation and survival of GBM cells. Also, it was revealed that NF-κB inhibition using Bay 11-7082 enhanced the inhibitory effects of ATO on migration of GBM cells via suppressing the expression of NF-κB target genes such as TWIST, MMP2, ICAM-1, and cathepsin B. Furthermore, combination treatment of GBM cells with ATO and Bay 11-7082 significantly induce apoptotic cell death coupled with downregulation of NF-κB anti-apoptotic target genes including Bcl-2 and IAP family members. Conclusions: Altogether, these findings suggest that combination therapy with ATO and Bay 11-7082 may be a promising strategy for the treatment of GBM.

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Targeting of EGFR increase anti-cancer effects of arsenic trioxide: Promising treatment for glioblastoma multiform

Cited by 18 publications

References 62 publications

Arsenic trioxide as a novel anti-glioma drug: a review

Arsenic trioxide as a novel anti-glioma drug: a review

Arsenic trioxide and Erlotinib loaded in RGD‐modified nanoliposomes for targeted combination delivery to PC3 and PANC‐1 cell lines

Blockade of Nuclear Factor-Κb (NF-Κb) Pathway Using Bay 11-7082 Enhances Arsenic Trioxide-Induced Antiproliferative Activity in U87 Glioblastoma Cells

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