Triggered ferroptotic polymer micelles for reversing multidrug resistance to chemotherapy

Gao, Min; Deng, Jian Hong; Liu, Fang; Fan, Aiping; Wang, Yujuan; Wu, Hsiao-Ming; Ding, Dan; Kong, Deling; Wang, Zheng; Peer, Dan; Zhao, Yanjun

doi:10.1016/j.biomaterials.2019.119486

Cited by 169 publications

(131 citation statements)

References 55 publications

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“…In addition to nanotherapeutics, Gao and colleagues reported another new method to overcome multidrug resistance in the treatment of cancer through tailored ferroptotic micelles, which consist of ferroptosis inducers with arachidonic acid-conjugated amphiphilic copolymers, opening a new horizon for treating drug-resistant tumors (129). Exosomes have become popular as drug carriers with low immunogenicity, high efficiency, and high biocompatibility.…”

Section: Ferroptosis-driven Nanotherapeutics and Other Novel Waysmentioning

confidence: 99%

Ferroptosis in Cancer Treatment: Another Way to Rome

Luo

et al. 2020

Front. Oncol.

124

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Ferroptosis is a newly described type of programmed cell death and intensively related to both maintaining homeostasis and the development of diseases, especially cancers. Inducing ferroptosis leads to mitochondrial dysfunction and toxic lipid peroxidation in cells, which plays a pivotal role in suppressing cancer growth and progression. Here, we reviewed the existing studies about the molecular mechanisms of ferroptosis involved in different antitumor treatments, such as chemotherapy, targeted therapy, radiotherapy, and immunotherapy. We focused in particular on the distinct combinatorial therapeutic effects such as the synergistic sensitization effect and the drug-resistance reversal achieved when using ferroptosis inducers with conventional cancer therapy. Finally, we discussed the challenges and opportunities in clinical applications of ferroptosis. The application of nanotechnolgy and other novel technologies may provide a new direction in ferroptosis-driven cancer therapies.

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Section: Ferroptosis-driven Nanotherapeutics and Other Novel Waysmentioning

confidence: 99%

Ferroptosis in Cancer Treatment: Another Way to Rome

Luo

et al. 2020

Front. Oncol.

124

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“…Then MCF‐7 cells treated respectively with the two complexes were investigated for ferroptosis‐associated markers or events under hypoxia [38] . Lipid peroxide accumulation, which was a characteristic of ferroptosis caused by Fe 2+ promoting overproduction of hydroxyl radicals, [39, 40] was then monitored using C11‐BODIPY as a lipid peroxide probe [41] . Confocal imaging disclosed that both Ir III complexes enhanced the probe fluorescence remarkably upon light irradiation under hypoxia (Figure 4 a,b), implying the obvious lipid peroxide accumulation.…”

Section: Resultsmentioning

confidence: 99%

Ferroptosis Photoinduced by New Cyclometalated Iridium(III) Complexes and Its Synergism with Apoptosis in Tumor Cell Inhibition

et al. 2021

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Limited therapeutic efficacy to hypoxic and refractory solid tumors has hindered the practical application of photodynamic therapy(PDT). Tw on ew benzothiophenylisoquinoline (btiq)-derived cyclometalated Ir III complexes, IrL1 and MitoIrL2,w ere constructed as potent photosensitizers, with the latter being designed for mitochondria accumulation. Both complexes demonstrated at ype IP DT process and caused photoinduced ferroptosis in tumor cells under hypoxia. This ferroptosis featured lipid peroxide accumulation, mitochondria shrinkage,d own-regulation of glutathione peroxidase 4(GPX4), and ferrostatin-1 (Fer-1)-inhibited cell death. Upon photoirradiation under hypoxia, mitochondria targeting MitoIrL2 caused mitochondria membrane potential (MMP) collapse,A TP production suppression, and induced cell apoptosis.T he synergetic effect of ferroptosis and apoptosis causes MitoIrL2 to outperform IrL1 in inhibiting the growth of MCF-7, PANC-1, MDA-MB-231 cells and multicellular spheroids.T his study demonstrates the first example of ferroptosis induced by photosensitizing Ir III complexes.Moreover,t he synergism of ferroptosis and apoptosis provides ap romising approach for combating hypoxics olid tumors through type IP DT processes.

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“…Thereinto, epithelial-mesenchymal transition (EMT) is the best-known mechanism for cell plasticity, encompassing loss of cell-cell junction, increased fibroid morphology, extracellular matrix-associated migration and resistance to apoptosis (28). Increasing data suggested that EMT exerts an essential influence on the emergence of persister cells (29,30). Overall, this genetic profiling of DTP corresponds to minimal residual disease in clinic, which represents as a transitory stage between initial response and progressive recurrence.…”

Section: Discussionmentioning

confidence: 99%

Gene Panel of Persister Cells as a Prognostic Indicator for Tumor Repopulation After Radiation

et al. 2020

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Tumor repopulation during cycles of radiotherapy limits the radio-response in ensuing cycles and causes failure of treatment. It is thus of vital importance to unveil the mechanisms underlying tumor repopulating cells. Increasing evidence suggests that a subpopulation of drug-tolerant persister cancer cells (DTPs) could survive the cytotoxic treatment and resume to propagate. Whether these persister cells contribute to development of radio-resistance remains elusive. Based on the genetic profiling of DTPs by integrating datasets from Gene Expression Omnibus database, this study aimed to provide novel insights into tumor-repopulation mediated radio-resistance and identify predictive biomarkers for radio-response in clinic. A prognostic risk index, grounded on four persister genes (LYNX1, SYNPO, GADD45B, and PDLIM1), was constructed in non-small-cell lung cancer patients from The Cancer Genome Atlas Program (TCGA) using stepwise Cox regression analysis. Weighted gene co-expression network analysis further confirmed the interaction among persister-gene based risk score, radio-response and overall survival time. In addition, the predictive role of risk index was validated in vitro and in other types of TCGA patients. Gene set enrichment analysis was performed to decipher the possible biological signaling, which indicated that two forces behind persister cells, stress response and survival adaptation, might fuel the tumor repopulation after radiation. Targeting these persister cells may represent a new prognostic and therapeutic approach to enhance radio-response and prevent radio-resistance induced by tumor repopulation.

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Triggered ferroptotic polymer micelles for reversing multidrug resistance to chemotherapy

Cited by 169 publications

References 55 publications

Ferroptosis in Cancer Treatment: Another Way to Rome

Ferroptosis in Cancer Treatment: Another Way to Rome

Ferroptosis Photoinduced by New Cyclometalated Iridium(III) Complexes and Its Synergism with Apoptosis in Tumor Cell Inhibition

Gene Panel of Persister Cells as a Prognostic Indicator for Tumor Repopulation After Radiation

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