TRAIL in oncology: From recombinant TRAIL to nano- and self-targeted TRAIL-based therapies

Dianat‐Moghadam, Hassan; Heidarifard, Maryam; Mahari, Amir; Shahgolzari, Mehdi; Keshavarz, Mohsen; Nouri, Mohammad; Amoozgar, Zohreh

doi:10.1016/j.phrs.2020.104716

Cited by 53 publications

(31 citation statements)

References 169 publications

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“…Apart from EV directing, receptor-ligand interactions may supposedly trigger the expected biological effects in targeted cells. For instance, tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-expressing EVs may potentially activate apoptosis in targeted tumor cells [ 104 ]. Similar pro-apoptotic effect can be induced by FasL-expressing EVs.…”

Section: Perspectives In Manipulating Evs For Therapeutic Applicatmentioning

confidence: 99%

Perspectives in Manipulating EVs for Therapeutic Applications: Focus on Cancer Treatment

Nazimek

Bryniarski

2020

IJMS

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Extracellular vesicles (EVs) receive special attention from oncologists due to their assumed usefulness as prognostic markers, vaccines to induce anti-cancer immune response, and physiological delivery tools. The latter application, which supports the reduction of side effects of treatment, is still fraught with many challenges, including established methods for loading EVs with selected cargo and directing them towards target cells. EVs could be loaded with selected cargo either in vitro using several physicochemical techniques, or in vivo by modification of parental cell, which may have an advantage over in vitro procedures, since some of them significantly influence EVs’ properties. Otherwise, our research findings suggest that EVs could be passively supplemented with micro RNAs (miRNAs) or miRNA antagonists to induce expected biological effect. Furthermore, our observations imply that antigen-specific antibody light chains could coat the surface of EVs to increase the specificity of cell targeting. Finally, the route of EVs’ administration also determines their bioavailability and eventually induced therapeutic effect. Besides, EV membrane lipids may possibly possess immune adjuvant activity. The review summarizes the current knowledge on the possibilities to manipulate EVs to use them as a delivery tool, with the special emphasis on anti-cancer therapy.

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Section: Perspectives In Manipulating Evs For Therapeutic Applicatmentioning

confidence: 99%

Perspectives in Manipulating EVs for Therapeutic Applications: Focus on Cancer Treatment

Nazimek

Bryniarski

2020

IJMS

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“… 22 , 23 Thus, TRAIL-based therapies have been applied in clinical trials and have shown minimal adverse effects for patients with several kinds of tumors, but little therapeutic efficacy as monotherapy due to poor circulation half-life, inefficient tumor targeting, and TRAIL resistance. 21 , 24 , 25 Nanoparticulate delivery systems hold promise for eliminating the TRAIL delivery barriers in vivo to facilitate tumor ablation. 21 , 26–28 For instance, TRAIL and transferrin were modified onto the surface of human serum albumin nanoparticles (NPs) containing doxorubicin (Dox) to induce various types of tumor cells apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Engineering of Neutrophil Membrane Camouflaging Nanoparticles Realizes Targeted Drug Delivery for Amplified Antitumor Therapy

Wang¹,

Gu²,

Ouyang³

et al. 2021

IJN

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Purpose Although the neutrophil membrane (NM)-based nanoparticulate delivery system has exhibited rapid advances in tumor targeting stemmed from the inherited instinct, the antitumor effect requires further improvement due to inefficient cellular internalization in the absence of specific interactions between NM-coated nanoparticles and tumor cells. Methods Herein, we fabricated drug-paclitaxel loaded NM camouflaging nanoparticles (TNM-PN) modified with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), favorable for the cellular internalization. Results The results showed that TNM-PN exerted a significant cytotoxicity to tumor cells by TRAIL-mediated endocytosis and strong adhesion to inflamed endothelial cells in vitro. Due to TRAIL modification as well as the adhesive interactions between neutrophil and inflamed tumor vascular endothelial cells, tumors in TNM-PN group exhibited almost 2-fold higher fluorescence intensities than that of NM camouflaging nanoparticles and 3-fold higher than that of bare nanoparticles, respectively. Significant tumor inhibition and survival rates of mice were achieved in TNM-PN group as a consequence of prolonged blood circulations to 48 h and preferential tumor accumulations, which was ascribed to targeting adhesion originated from NM to immune evasion and subsequent excellent cellular internalization. Conclusion The research unveiled a novel strategy of amplifying cellular internalization based on NM coating nanotechnology to boost antitumor efficacy.

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“…[1] Tumor-necrosis-factorrelated apoptosis-inducing ligand (TRAIL) is able to induce canonical apoptotic cell death in cancer cells without causing toxicity, and therefore is considered as an attractive agent for cancer therapy. [2] However, majority of cancer cell lines and primary tumors such as non-small cell lung cancer (NSCLC) are TRAIL resistant, [3] resulting in a universal treatment failure of late-stage cancer patients by TRAIL. [4,5] Increasing evidences indicated that TRAIL death receptors (DRs) are functionally defective in different types of cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Curcumol Overcomes TRAIL Resistance of Non‐Small Cell Lung Cancer by Targeting NRH:Quinone Oxidoreductase 2 (NQO2)

Zhang

Zhou

et al. 2020

Advanced Science

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Resistance to tumor-necrosis-factor-related apoptosis-inducing ligand (TRAIL) of cancer cell remains a key obstacle for clinical cancer therapies. To overcome TRAIL resistance, this study identifies curcumol as a novel safe sensitizer from a food-source compound library, which exhibits synergistic lethal effects in combination with TRAIL on non-small cell lung cancer (NSCLC). SILAC-based cellular thermal shift profiling identifies NRH:quinone oxidoreductase 2 (NQO2) as the key target of curcumol. Mechanistically, curcumol directly targets NQO2 to cause reactive oxygen species (ROS) generation, which triggers endoplasmic reticulum (ER) stress-C/EBP homologous protein (CHOP) death receptor (DR5) signaling, sensitizing NSCLC cell to TRAIL-induced apoptosis. Molecular docking analysis and surface plasmon resonance assay demonstrate that Phe178 in NQO2 is a critical site for curcumol binding. Mutation of Phe178 completely abolishes the function of NQO2 and augments the TRAIL sensitization. This study characterizes the functional role of NQO2 in TRAIL resistance and the sensitizing function of curcumol by directly targeting NQO2, highlighting the potential of using curcumol as an NQO2 inhibitor for clinical treatment of TRAIL-resistant cancers.

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TRAIL in oncology: From recombinant TRAIL to nano- and self-targeted TRAIL-based therapies

Cited by 53 publications

References 169 publications

Perspectives in Manipulating EVs for Therapeutic Applications: Focus on Cancer Treatment

Perspectives in Manipulating EVs for Therapeutic Applications: Focus on Cancer Treatment

Engineering of Neutrophil Membrane Camouflaging Nanoparticles Realizes Targeted Drug Delivery for Amplified Antitumor Therapy

Curcumol Overcomes TRAIL Resistance of Non‐Small Cell Lung Cancer by Targeting NRH:Quinone Oxidoreductase 2 (NQO2)

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