Novel imatinib-loaded silver nanoparticles for enhanced apoptosis of human breast cancer MCF-7 cells

Shandiz, Seyed Ataollah Sadat; Ardestani, Mehdi Shafiee; Shahbazzadeh, Delavar; Assadi, Artin; Cohan, Reza Ahangari; Asgary, Vahid; Salehi, Soheil

doi:10.1080/21691401.2016.1202257

Cited by 73 publications

(37 citation statements)

References 28 publications

(27 reference statements)

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“…Our previous work showed that Tap73/DNp73 plays an important role in regulating apoptosis via mitochondrial pathway [29,30]. Apoptosis is regulated by pro-apoptotic and antiapoptotic effectors that involve a different pathway, such as Bcl-2 and caspase pathways which serve as important regulators of apoptosis pathways [42]. In our previous work, the magnitude of radiation effects in mouse testis evoked by carbon ion irradiation was marked by morphology changes, significant rise in apoptotic cells, up-regulation the ratio of pro-apoptotic Tap73/anti-apoptotic DNp73, as well as alterations of crucial mediator of the mitochondrial pathway [29].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of SF3b1 by pladienolide B evokes cycle arrest, apoptosis induction and p73 splicing in human cervical carcinoma cells

Zhang

Chen

Yan

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Pladienolide B is a potent cancer cell growth inhibitor that targets the SF3b1 subunit of the spliceosome. There is considerable interest in the compound as a tool to study SF3b1 function in cancer. However, so far little information is available on the molecular mechanism of SF3b1 eliciting apoptosis in cancer cells. Here, we investigated the molecular mechanism of SF3b1 eliciting apoptosis in human cervical carcinoma cells. We demonstrated that inhibition of SF3b1 by pladienolide B inhibited proliferation of HeLa cells at low nanomolar concentrations in a dose-and time-dependent manner. It also induced G2/M phase arrest and significant rise of apoptotic cells. Moreover, it is indicated that inhibition of SF3b1 by pladienolide B induced Tap73/DNp73 expression and consequently down-regulated Bax/Bcl-2 ratio, cytochrome c release and caspase-3 expression. Thus, our results showed that SF3b1 plays a pivotal role in cycle arrest, apoptosis induction, and p73 splicing in human cervical carcinoma cells, suggesting that SF3b1 could be used as a potential candidate for cervical cancer therapy.

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Section: Discussionmentioning

confidence: 99%

Inhibition of SF3b1 by pladienolide B evokes cycle arrest, apoptosis induction and p73 splicing in human cervical carcinoma cells

Zhang

Chen

Yan

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…Apoptosis induction in E. coli-infected macrophages by pure and encapsulated HHC10 peptide was evaluated by Annexin V-PI method using by flow cytometry [29,30]. It was investigated by staining macrophages with FITC-conjugated Annexin V-PI apoptosis kit according to the manufacturer protocol (Sigma).…”

Section: Apoptosis Assaymentioning

confidence: 99%

Nano-encapsulated HHC10 host defense peptide (HDP) reduces the growth of Escherichia coli via multimodal mechanisms

Sharma

Vaghasiya

Ray

et al. 2018

Artificial Cells, Nanomedicine, and Biotechnology

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The eradication of several pathogenic drug resistant "Superbug" such as Escherichia coli became difficult especially in chronic infections using existing antibiotics due to the emergence of antibiotic resistance. Owing to their unique antibacterial properties, host defense peptides (HDP) have gained significant attention to combat colonization of bacteria. This study aims designing delivery systems for HHC10 peptide to target bacteria inside the cells might be a promising approach by protecting from degradation, controlling the release, enhancing the susceptibility of target microbes and improving bioavailability. Nano-formulated HHC10 was evaluated for its efficacy (CFU assay) and possible mechanism of action (membrane interaction and apoptosis) against E. coli. Dose-dependent inhibition of E. coli growth is observed for nano-encapsulated and bare HHC10 and encapsulated form remain non-toxic to macrophage mouse cells (RAW264.6) up to 20 μM. Mechanistic analyses using transmission electron microscopy and flow cytometry techniques revealed that bactericidal activity of HHC10-NP progresses via a multimodal mechanism of bacterial cell death by cell-membrane lysis on direct interaction with bacteria while through induction of the apoptotic death pathway inside the host cells. These results offer an insight on future strategies for the development and application of antimicrobial peptides as antibacterial alternatives. [Formula: see text] Controlled delivery of HHC10 peptide from PLGA-NP kills bacteria by two different mechanism: (i) direct killing: HHC10 disintegrate the cell membrane of bacteria by electrostatic interactions and (ii) indirect killing: induction of apoptosis in bacteria infect cells.

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“…Recent studies have shown that the expression of GSH and subunits of two GSH-synthesizing enzymes along with the associated mRNA expression are downregulated in human liver cells. These responses were accompanied by mitochondrial membrane disruption through the downregulation of Bcl-2 protein expression and concomitant upregulation of Bax protein expression [21,37]. The opening of the mitochondrial membrane is inhibited and stimulated by Bcl-2 and Bax, respectively.…”

Section: Phagocytosis and Ros Generationmentioning

confidence: 99%

Microcellular Environmental Regulation of Silver Nanoparticles in Cancer Therapy: A Critical Review

Ganesan

Jang

Suh

et al. 2020

Cancers

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Silver nanoparticles (AgNPs) play significant roles in various cancer cells such as functional heterogeneity, microenvironmental differences, and reversible changes in cell properties (e.g., chemotherapy). There is a lack of targets for processes involved in tumor cellular heterogeneity, such as metabolic clampdown, cytotoxicity, and genotoxicity, which hinders microenvironmental biology. Proteogenomics and chemical metabolomics are important tools that can be used to study proteins/genes and metabolites in cells, respectively. Chemical metabolomics have many advantages over genomics, transcriptomics, and proteomics in anticancer therapy. However, recent studies with AgNPs have revealed considerable genomic and proteomic changes, particularly in genes involved in tumor suppression, apoptosis, and oxidative stress. Metabolites interact biochemically with energy storage, neurotransmitters, and antioxidant defense systems. Mechanobiological studies of AgNPs in cancer metabolomics suggest that AgNPs may be promising tools that can be exploited to develop more robust and effective adaptive anticancer therapies. Herein, we present a proof-of-concept review for AgNPs-based proteogenomics and chemical metabolomics from various tumor cells with the help of several technologies, suggesting their promising use as drug carriers for cancer therapy.

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Novel imatinib-loaded silver nanoparticles for enhanced apoptosis of human breast cancer MCF-7 cells

Cited by 73 publications

References 28 publications

Inhibition of SF3b1 by pladienolide B evokes cycle arrest, apoptosis induction and p73 splicing in human cervical carcinoma cells

Inhibition of SF3b1 by pladienolide B evokes cycle arrest, apoptosis induction and p73 splicing in human cervical carcinoma cells

Nano-encapsulated HHC10 host defense peptide (HDP) reduces the growth of Escherichia coli via multimodal mechanisms

Microcellular Environmental Regulation of Silver Nanoparticles in Cancer Therapy: A Critical Review

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