Chemotherapeutic and targeted drugs-induced immunogenic cell death in cancer models and antitumor therapy: An update review

Zhang, Jiaqi; Gu, Xi; Liu, Yang; Hu, Yanrong; Jiang, Yi; Zhang, Zhenyong

doi:10.3389/fphar.2023.1152934

Cited by 31 publications

(17 citation statements)

References 172 publications

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“…In parallel, recent studies have demonstrated that specific chemotherapeutic drugs, such as doxorubicin, camptothecin, oxaliplatin and paclitaxel (Ptx) can induce immunogenic cell death (ICD) ( Lau et al, 2020 ; Vanmeerbeek et al, 2020 ; Zhai et al, 2023 ). During ICD, dying cancer cells release damage-associated molecular patterns (DAMPs) and danger signals, such as calreticulin (CRT), adenosine 5′-triphosphate (ATP) and the high-mobility group box 1 protein (HMGB1), which collectively recruit phagocytic cells and activate the immune system at the tumor site.…”

Section: Introductionmentioning

confidence: 99%

HSA-nanobinders crafted from bioresponsive prodrugs for combined cancer chemoimmunotherapy–an in vitro exploration

Tubertini,

Menilli,

Milani

et al. 2024

Front. Chem.

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Introduction: Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer still lacking effective treatment options. Chemotherapy in combination with immunotherapy can restrict tumor progression and repolarize the tumor microenvironment towards an anti-tumor milieu, improving clinical outcome in TNBC patients. The chemotherapeutic drug paclitaxel has been shown to induce immunogenic cell death (ICD), whereas inhibitors of the indoleamine 2,3- dioxygenase 1 (IDO1) enzyme, whose expression is shared in immune regulatory and tumor cells, have been revealed to enhance the anti-tumor immune response. However, poor bioavailability and pharmacokinetics, off-target effects and hurdles in achieving therapeutic drug concentrations at the target tissue often limit the effectiveness of combination therapies.Methods: This work describes the development of novel biomimetic and carrier-free nanobinders (NBs) loaded with both paclitaxel and the IDO1 inhibitor NLG919 in the form of bioresponsive and biomimetic prodrugs. A fine tuning of the preparation conditions allowed to identify NB@5 as the most suitable nanoformulation in terms of reproducibility, stability and in vitro effectiveness.Results and discussion: Our data show that NB@5 effectively binds to HSA in cell-free experiments, demonstrating its protective role in the controlled release of drugs and suggesting the potential to exploit the protein as the endogenous vehicle for targeted delivery to the tumor site. Our study successfully proves that the drugs encapsulated within the NBs are preferentially released under the altered redox conditions commonly found in the tumor microenvironment, thereby inducing cell death, promoting ICD, and inhibiting IDO1.

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Section: Introductionmentioning

confidence: 99%

HSA-nanobinders crafted from bioresponsive prodrugs for combined cancer chemoimmunotherapy–an in vitro exploration

Tubertini,

Menilli,

Milani

et al. 2024

Front. Chem.

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“…[ 30 ] HMGB1 is a nuclear protein that acts as an immune adjuvant by activating dendritic cells and promoting the recruitment of immune cells to the tumor microenvironment. [ 31 ] HMGB1 stimulates the production of pro‐inflammatory cytokines and chemokines, activating antigen‐presenting cells and initiating an adaptive immune response. [ 32 ] The interaction between HMGB1 and CD40 leads to the increased expression of major histocompatibility complex (MHC) class molecules and costimulatory molecules such as CD80 and CD86.…”

Section: Resultsmentioning

confidence: 99%

A “One Arrow Three Eagle” Strategy to Improve CM‐272 Primed Bladder Cancer Immunotherapy

Liu,

Yang,

et al. 2023

Advanced Materials

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Immunotherapy using an immune‐checkpoint blockade has significantly improved its therapeutic effects. CM‐272, which is a novel epigenetic inhibitor of G9a, induces immunogenic cell death (ICD) for recovering the sensitivity to anti‐PD‐1 antibodies; however, the efficacy of CM‐272 is greatly limited by promoting the transcription activity of HIF‐1α to form a hypoxic environment. Here, a Fe3+‐based nanoscale metal–organic framework (MIL‐53) is used to load CM‐272 (ultra‐high loading rate of 56.4%) for realizing an MIL‐53@CM‐272 nanoplatform. After entering bladder cancer cells, Fe3+ not only promotes the decomposition of H2O2 into O2 for O2‐compensated sonodynamic therapy but reduces the high level of glutathione in the tumor microenvironment (TME) for enhancing reactive oxygen species, including ferroptosis and apoptosis. MIL‐53 carriers can be degraded in response to the TME, accelerating the release of CM‐272, which helps achieve the maximum effectiveness in an O2‐sufficient TME by attenuating drug resistance. Furthermore, MIL‐53@CM‐272 enhances dendritic cell maturation and synergistically combines it with an anti‐programmed cell death protein 1 antibody during the study of immune‐related pathways in the transcriptomes of bladder cancer cells using RNA‐seq. This study presents the first instance of amalgamating nanomedicine with CM‐272, inducing apoptosis, ferroptosis, and ICD to achieve the “one arrow three eagle” effect.

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“…Immunogenicity can then be readily restored by adding recombinant CRT protein back to the plasma membrane surface 50 . Thus, translocation of CRT from the ER is a key determinant of anticancer immune responses, which has been exploited as a target mechanism for immunogenic chemotherapy 26,27,51 .…”

Section: Discussionmentioning

confidence: 99%

Ferroptosis and HMGB2 induced calreticulin translocation required for immunogenic cell death are controlled by the nuclear exporter XPO1

Blair,

Fan,

Gillespie

et al. 2024

Preprint

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Cisplatin and oxaliplatin cause the secretion of high mobility group box 1 (HMGB1) from cancer cells, which is necessary for initiation of immunogenic cell death (ICD). Calreticulin (CRT) translocation from the endoplasmic reticulum to the plasma membrane is also required; oxaliplatin induces this translocation but cisplatin does not. We have discovered that oxaliplatin causes the secretion of both HMGB1 and HMGB2 from the nucleus into the extracellular milieu. We previously showed that cisplatin mediated secretion of HMGB1 is controlled by the nuclear exporter XPO1 (chromosomal maintenance 1; CRM1). We now find that XPO1 regulates oxaliplatin mediated secretion of both HMGB1 and HMGB2. XPO1 inhibition causes nuclear accumulation of both proteins, inhibition of oxaliplatin-mediated ferroptosis of colon cancer cells, and inhibition of CRT translocation to the plasma membrane of lung and colon cancer cells. Incubation of cancer cells with cell targeted (CT)-HMGB2 confirmed that HMGB2 is responsible for translocation of CRT to the plasma membrane. CT-HMGB2 is three orders of magnitude more potent than oxaliplatin at inducing CRT translocation. Inhibition of HMGB1 and HMGB2 secretion and/or their activation of nuclear factor-kappa B (NF-kB) has potential utility for treating cardiovascular, and neurodegenerative diseases; whereas CT-HMGB2 could augment therapeutic approaches to cancer treatment.

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Chemotherapeutic and targeted drugs-induced immunogenic cell death in cancer models and antitumor therapy: An update review

Cited by 31 publications

References 172 publications

HSA-nanobinders crafted from bioresponsive prodrugs for combined cancer chemoimmunotherapy–an in vitro exploration

HSA-nanobinders crafted from bioresponsive prodrugs for combined cancer chemoimmunotherapy–an in vitro exploration

A “One Arrow Three Eagle” Strategy to Improve CM‐272 Primed Bladder Cancer Immunotherapy

Ferroptosis and HMGB2 induced calreticulin translocation required for immunogenic cell death are controlled by the nuclear exporter XPO1

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