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  1. Article: The many metabolic sources of acetyl-CoA to support histone acetylation and influence cancer progression.

    Feron, Olivier

    Annals of translational medicine

    2020  Volume 7, Issue Suppl 8, Page(s) S277

    Language English
    Publishing date 2020-01-03
    Publishing country China
    Document type Editorial ; Comment
    ZDB-ID 2893931-1
    ISSN 2305-5847 ; 2305-5839
    ISSN (online) 2305-5847
    ISSN 2305-5839
    DOI 10.21037/atm.2019.11.140
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  2. Article ; Online: A novel approach to pH-Responsive targeted cancer Therapy: Inhibition of FaDu cancer cell proliferation with a pH low insertion Peptide-Conjugated DGAT1 inhibitor.

    Deskeuvre, Marine / Lan, Junjie / Messens, Joris / Riant, Olivier / Feron, Olivier / Frédérick, Raphaël

    International journal of pharmaceutics

    2024  Volume 657, Page(s) 124132

    Abstract: ... strategy. Efficient inhibition of diacylglycerol O-transferase 1 (DGAT1) can block fatty acid (FA) storage ...

    Abstract Targeting enzymes involved in lipid metabolism is increasingly recognized as a promising anticancer strategy. Efficient inhibition of diacylglycerol O-transferase 1 (DGAT1) can block fatty acid (FA) storage. This, in turn, triggers an increase in free polyunsaturated FA concentration, leading to peroxidation and ferroptosis. In this study, we report the development of a pH-sensitive peptide (pHLIP)-drug conjugate designed to selectively deliver DGAT1 inhibitors to cancer cells nested within the acidic microenvironment of tumors. We utilized two previously established pHLIP sequences for coupling with drugs. The study of DGAT1 conjugates in large unilamellar vesicles (LUVs) of different compositions did not reveal enhanced pH-dependent insertion compared to POPC LUVs. However, using in vitro 3D tumor spheroids, significant antiproliferative effects were observed upon exposure to pHLIP-T863 (DGAT1 inhibitor) conjugates, surpassing the inhibitory activity of T863 alone. In conclusion, our study provides the first evidence that pHLIP-based conjugates with DGAT1 inhibitors have the potential to specifically target the acidic compartment of tumors. Moreover, it sheds light on the limitations of LUV models in capturing the pH-dependency of such conjugates.
    Language English
    Publishing date 2024-04-17
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 428962-6
    ISSN 1873-3476 ; 0378-5173
    ISSN (online) 1873-3476
    ISSN 0378-5173
    DOI 10.1016/j.ijpharm.2024.124132
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  3. Article: Editorial: Insights in pharmacology of anti-cancer drugs: 2021.

    Sancho, Patricia / Feron, Olivier

    Frontiers in pharmacology

    2022  Volume 13, Page(s) 1062640

    Language English
    Publishing date 2022-10-21
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2022.1062640
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  4. Article ; Online: Editorial: Targeting glucose metabolism in cancer immunity and immunotherapy.

    Feron, Olivier / Chang, Chih-Hao / Végran, Frédérique

    Frontiers in immunology

    2023  Volume 14, Page(s) 1171274

    MeSH term(s) Humans ; Neoplasms/therapy ; Neoplasms/metabolism ; Carbohydrate Metabolism ; Glucose/metabolism ; Immunotherapy
    Chemical Substances Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2023-03-08
    Publishing country Switzerland
    Document type Editorial ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1171274
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  5. Article: Discovery of Mitochondrial Complex I Inhibitors as Anticancer and Radiosensitizer Drugs Based on Compensatory Stimulation of Lactate Release.

    Lan, Junjie / Cadassou, Octavia / Corbet, Cyril / Riant, Olivier / Feron, Olivier

    Cancers

    2022  Volume 14, Issue 21

    Abstract: Cancer cells may stimulate glycolytic flux when O ...

    Abstract Cancer cells may stimulate glycolytic flux when O
    Language English
    Publishing date 2022-11-06
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers14215454
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  6. Article: The impact of macrophages on endothelial cells is potentiated by cycling hypoxia: Enhanced tumor inflammation and metastasis.

    Delprat, Victor / Huart, Camille / Feron, Olivier / Soncin, Fabrice / Michiels, Carine

    Frontiers in oncology

    2022  Volume 12, Page(s) 961753

    Abstract: Cycling hypoxia (cyH), neo-angiogenesis, and tumor-associated macrophages are key features of the tumor microenvironment. In this study, we demonstrate that cyH potentiates the induction by unpolarized and M1-like macrophages of endothelial inflammatory ... ...

    Abstract Cycling hypoxia (cyH), neo-angiogenesis, and tumor-associated macrophages are key features of the tumor microenvironment. In this study, we demonstrate that cyH potentiates the induction by unpolarized and M1-like macrophages of endothelial inflammatory phenotype and adhesiveness for monocytes and cancer cells. This process triggers a positive feedback loop sustaining tumor inflammation. This work opens the door for innovative therapeutic strategies to treat tumor inflammation and metastasis. In cancers, the interaction between macrophages and endothelial cells (ECs) regulates tumor inflammation and metastasis. These cells are both affected by cycling hypoxia (cyH), also called intermittent hypoxia, a feature of the tumor microenvironment. cyH is also known to favor tumor inflammation and metastasis. Nonetheless, the potential impact of cyH on the dialog between macrophages and ECs is still unknown. In this work, the effects of unpolarized, M1-like, and M2-like macrophages exposed to normoxia, chronic hypoxia (chH), and cyH on endothelial adhesion molecule expression, pro-inflammatory gene expression, and EC adhesiveness for monocytes and cancer cells were investigated. cyH increased the ability of unpolarized and M1-like macrophages to induce EC inflammation and to increase the expression of the EC endothelial adhesion molecule ICAM1, respectively. Unpolarized, M1-like, and M2-like macrophages were all able to promote EC adhesive properties toward cancer cells. Furthermore, the ability of macrophages (mostly M1-like) to shift EC phenotype toward one allowing cancer cell and monocyte adhesion onto ECs was potentiated by cyH. These effects were specific to cyH because they were not observed with chH. Together, these results show that cyH amplifies the effects of macrophages on ECs, which may promote tumor inflammation and metastasis.
    Language English
    Publishing date 2022-09-28
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2022.961753
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  7. Article ; Online: Immunogenic Cell Death and Role of Nanomaterials Serving as Therapeutic Vaccine for Personalized Cancer Immunotherapy.

    Catanzaro, Elena / Feron, Olivier / Skirtach, André G / Krysko, Dmitri V

    Frontiers in immunology

    2022  Volume 13, Page(s) 925290

    Abstract: Immunogenic cell death (ICD) is a rapidly growing research area representing one of the emerging therapeutic strategies of cancer immunotherapy. ICD is an umbrella term covering several cell death modalities including apoptosis, necroptosis, ferroptosis ... ...

    Abstract Immunogenic cell death (ICD) is a rapidly growing research area representing one of the emerging therapeutic strategies of cancer immunotherapy. ICD is an umbrella term covering several cell death modalities including apoptosis, necroptosis, ferroptosis and pyroptosis, and is the product of a balanced combination of adjuvanticity (damage-associated molecular patterns and chemokines/cytokines) and antigenicity (tumor associated antigens). Only a limited number of anti-cancer therapies are available to induce ICD in experimental cancer therapies and even much less is available for clinical use. To overcome this limitation, nanomaterials can be used to increase the immunogenicity of cancer cells killed by anti-cancer therapy, which in themselves are not necessarily immunogenic. In this review, we outline the current state of knowledge of ICD modalities and discuss achievements in using nanomaterials to increase the immunogenicity of dying cancer cells. The emerging trends in modulating the immunogenicity of dying cancer cells in experimental and translational cancer therapies and the challenges facing them are described. In conclusion, nanomaterials are expected to drive further progress in their use to increase efficacy of anti-cancer therapy based on ICD induction and in the future, it is necessary to validate these strategies in clinical settings, which will be a challenging research area.
    MeSH term(s) Cell Death ; Immunogenic Cell Death ; Immunotherapy ; Nanostructures ; Neoplasms/therapy ; Vaccines
    Chemical Substances Vaccines
    Language English
    Publishing date 2022-06-30
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.925290
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  8. Article: Targeting M2 Macrophages with a Novel NADPH Oxidase Inhibitor.

    Dilly, Sébastien / Romero, Miguel / Solier, Stéphanie / Feron, Olivier / Dessy, Chantal / Slama Schwok, Anny

    Antioxidants (Basel, Switzerland)

    2023  Volume 12, Issue 2

    Abstract: ROS in cancer cells play a key role in pathways regulating cell death, stemness maintenance, and metabolic reprogramming, all of which have been implicated in resistance to chemo/ immunotherapy. Adjusting ROS levels to reverse the resistance of cancer ... ...

    Abstract ROS in cancer cells play a key role in pathways regulating cell death, stemness maintenance, and metabolic reprogramming, all of which have been implicated in resistance to chemo/ immunotherapy. Adjusting ROS levels to reverse the resistance of cancer cells without impairing normal cell functions is a new therapeutic avenue. In this paper, we describe new inhibitors of NADPH oxidase (NOX), a key enzyme in many cells of the tumor microenvironment. The first inhibitor, called Nanoshutter-1, NS1, decreased the level of tumor-promoting "M2" macrophages differentiated from human blood monocytes. NS1 disrupted the active NADPH oxidase-2 (NOX2) complex at the membrane and in the mitochondria of the macrophages, as shown by confocal microscopy. As one of the characteristics of tumor invasion is hypoxia, we tested whether NS1 would affect vascular reactivity by reducing ROS or NO levels in wire and pressure myograph experiments on isolated blood vessels. The results show that NS1 vasodilated blood vessels and would likely reduce hypoxia. Finally, as both NOX2 and NOX4 are key proteins in tumors and their microenvironment, we investigated whether NS1 would probe these proteins differently. Models of NOX2 and NOX4 were generated by homology modeling, showing structural differences at their C-terminal NADPH site, in particular in their last Phe. Thus, the NADPH site presents an unexploited chemical space for addressing ligand specificity, which we exploited to design a novel NOX2-specific inhibitor targeting variable NOX2 residues. With the proper smart vehicle to target specific cells of the microenvironment as TAMs, NOX2-specific inhibitors could open the way to new precision therapies.
    Language English
    Publishing date 2023-02-10
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox12020440
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  9. Article ; Online: Ex vivo

    Moghassemi, Saeid / Dadashzadeh, Arezoo / Camboni, Alessandra / Feron, Olivier / Azevedo, Ricardo Bentes / Amorim, Christiani A

    Human reproduction open

    2023  Volume 2023, Issue 2, Page(s) hoad005

    Abstract: Study question: Is it possible to purge leukemia cells from ovarian tissue (OT) fragments before transplantation?: Summary answer: Our photodynamic therapy (PDT) approach has been shown to efficiently destroy leukemia cells from tumor-infiltration ... ...

    Abstract Study question: Is it possible to purge leukemia cells from ovarian tissue (OT) fragments before transplantation?
    Summary answer: Our photodynamic therapy (PDT) approach has been shown to efficiently destroy leukemia cells from tumor-infiltration mimicking models (TIMs), indicating the feasibility of this technique to purge OT samples.
    What is known already: Autotransplantation of cryopreserved OT is the most suitable option to preserve fertility for prepubertal girls and women who require immediate cancer treatment. Up until now, more than 200 live births have already been reported after OT cryopreservation and transplantation. Leukemia is the 12th most common cancer in Europe among prepubertal girls and women of reproductive age and in 2020, the estimated number of new leukemia cases was higher than 33 000 in girls between 0 and 19 years old. Unfortunately, once their health has been restored, autotransplantation of cryopreserved OT for leukemia patients is not advised due to the high risk of transferring malignant cells back to the patient leading to leukemia recurrence.
    Study design size duration: To safely transplant the OT from leukemia patients and restore their fertility, our goal was to develop a PDT strategy to eliminate leukemia
    Participants/materials setting methods: After establishing the best ORN formulation, our PDT approach was used to eradicate HL60 cells from
    Main results and the role of chance: The
    Large scale data: N/A.
    Limitations reasons for caution: This study did not use OT fragments from leukemia patients, but TIMs created after injection of HL60 cells into OT from healthy patients. Therefore, while the results are promising, whether our PDT approach will be equally successful in eliminating malignant cells from leukemia patients remains to be assessed.
    Wider implications of the findings: Our results showed that the purging procedure causes no significant impairment effect on follicle development and tissue quality, suggesting that our novel PDT procedure could be a promising strategy to destroy leukemia cells in fragments of OT, allowing safe transplantation in cancer survivors.
    Study funding/competing interests: This study was supported by grants from the Fonds National de la Recherche Scientifique de Belgique (FNRS-PDR Convention grant number T.0004.20 awarded to C.A.A.); Fondation Louvain (awarded to C.A.A.; a Ph.D. scholarship awarded to S.M., as part of a legacy from Mr Frans Heyes, and a Ph.D. scholarship awarded to A.D. as part of a legacy from Mrs. Ilse Schirmer); and Foundation Against Cancer (grant number 2018-042 awarded to A.C.). The authors declare no competing interests.
    Language English
    Publishing date 2023-02-20
    Publishing country England
    Document type Journal Article
    ISSN 2399-3529
    ISSN (online) 2399-3529
    DOI 10.1093/hropen/hoad005
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  10. Article ; Online: Dealing with saturated and unsaturated fatty acid metabolism for anticancer therapy.

    Dierge, Emeline / Feron, Olivier

    Current opinion in clinical nutrition and metabolic care

    2019  Volume 22, Issue 6, Page(s) 427–433

    Abstract: Purpose of review: Although saturated fatty acid (FA) (SFA) and monounsaturated FA (MUFA) are synthesized in cancer cells from acetyl-CoA, polyunsaturated FAs (PUFAs) are necessarily obtained from diet. Depending on concentrations and metabolism, these ... ...

    Abstract Purpose of review: Although saturated fatty acid (FA) (SFA) and monounsaturated FA (MUFA) are synthesized in cancer cells from acetyl-CoA, polyunsaturated FAs (PUFAs) are necessarily obtained from diet. Depending on concentrations and metabolism, these different FAs may support tumor proliferation but also exert growth inhibitory effects. The mutual interplay between them also requires to integrate the FA oxidation component that may be concomitant with FA synthesis is cancer cells.
    Recent findings: New molecular mechanisms driving FA synthesis, lipotoxicity and anti-inflammatory activity of eicosanoids in mouse and human cancers were recently elicited. To block or take advantage of the above represent attractive perspectives of treatments to fight cancer progression.
    Summary: The various enzymatic reactions leading to SFA synthesis represent as many targets to prevent tumor growth. Ironically excess SFAs are per-se toxic for cancer cells and the introduction of a double bound to form MUFA is actually limiting lipotoxicity in cancer cells. Blocking stearoyl-CoA desaturase therefore represents another attractive modality. By contrast, dietary PUFAs may exert direct cytotoxic effects by promoting apoptosis or by generating anti-inflammatory eicosanoids. Altogether, these data point out the intricate relationship between SFA, MUFA and PUFA at the heart of the metabolism of proliferating cancer cells.
    MeSH term(s) Animals ; Antineoplastic Agents ; Apoptosis ; Dietary Fats/metabolism ; Eicosanoids ; Fatty Acids/biosynthesis ; Fatty Acids/metabolism ; Humans ; Mice ; Neoplasms/metabolism ; Neoplasms/physiopathology ; Neoplasms/therapy
    Chemical Substances Antineoplastic Agents ; Dietary Fats ; Eicosanoids ; Fatty Acids
    Language English
    Publishing date 2019-10-07
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1460178-3
    ISSN 1473-6519 ; 1363-1950
    ISSN (online) 1473-6519
    ISSN 1363-1950
    DOI 10.1097/MCO.0000000000000601
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