References of "Herfs, Michael"
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See detailUnveiling of a new role for DPF3 protein in cancer biology
Verrillo, Giulia ULiege; Hanache, Sarah ULiege; Duchemin, Amandine ULiege et al

Poster (2019, February)

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See detailHMGB1: a novel immunotherapeutic target
Herfs, Michael ULiege

Conference (2019, January 28)

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See detailComparative RNA sequencing reveals that HPV16 E6 abrogates the effect of E6*I on ROS metabolism
Paget-Bailly, Philippe; Meznad, Koceila; Bruyère, Diane ULiege et al

in Scientific Reports (2019)

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See detailHuman colon cancer cells highly express myoferlin to maintain a fit mitochondrial network and escape p53-driven apoptosis.
Rademaker, Gilles ULiege; Costanza, Brunella; Bellier, Justine ULiege et al

in Oncogenesis (2019)

Colon adenocarcinoma is the third most commonly diagnosed cancer and the second deadliest one. Metabolic reprogramming, described as an emerging hallmark of malignant cells, includes the predominant use ... [more ▼]

Colon adenocarcinoma is the third most commonly diagnosed cancer and the second deadliest one. Metabolic reprogramming, described as an emerging hallmark of malignant cells, includes the predominant use of glycolysis to produce energy. Recent studies demonstrated that mitochondrial electron transport chain inhibitor reduced colon cancer tumour growth. Accumulating evidence show that myoferlin, a member of the ferlin family, is highly expressed in several cancer types, where it acts as a tumour-promoter and participates in the metabolic rewiring towards oxidative metabolism. In this study, we showed that myoferlin expression in colon cancer lesions is associated with low patient survival and is higher than in non-tumoural adjacent tissue. Human colon cancer cells silenced for myoferlin exhibit a reduced oxidative phosphorylation activity associated with mitochondrial fission leading, ROS accumulation, decreased cell growth, and increased apoptosis. We observed the triggering of a DNA damage response culminating to a cell cycle arrest in wild-type p53 cells. The use of a p53 null cell line or a compound able to restore p53 activity (Prima-1) reverted the effects induced by myoferlin silencing, confirming the involvement of p53. The recent identification of a compound interacting with a myoferlin C2 domain and bearing anti-cancer potency identifies, together with our demonstration, this protein as a suitable new therapeutic target in colon cancer. [less ▲]

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See detailEMT is associated with an epigenetic signature of ECM remodeling genes
Peixoto, P.; Etcheverry, A.; Aubry, M. et al

in Cell Death and Disease (2019), 10(3),

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See detailMethylglyoxal, a glycolysis metabolite, triggers metastasis through MEK/ERK/SMAD1 pathway activation in breast cancer
Nokin, Marie-Julie ULiege; Bellier, Justine ULiege; Durieux, Florence et al

in Breast Cancer Research (2019), 21(1

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See detailClassic Vulvar Intraepithelial Neoplasia With Superimposed Lichen Simplex Chronicus: A Unique Variant Mimicking Differentiated Vulvar Intraepithelial Neoplasia.
Watkins, Jaclyn; Yang, Eric; Crum, Christopher et al

in International Journal of Gynecological Pathology (2019), 38(2)

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See detailMicroproteomic Profiling of High-Grade Squamous Intraepithelial Lesion of the Cervix: Insight into Biological Mechanisms of Dysplasia and New Potential Diagnostic Markers
Pottier, Charles ULiege; Kriegsmann, M.; Alberts, D. et al

in Proteomics. Clinical Applications (2019), 13(1)

Purpose: High-grade squamous intraepithelial lesion (HSIL) is a known precursor for squamous cell carcinoma of uterine cervix. Although it is known that SILs are associated to infection by human ... [more ▼]

Purpose: High-grade squamous intraepithelial lesion (HSIL) is a known precursor for squamous cell carcinoma of uterine cervix. Although it is known that SILs are associated to infection by human papillomavirus, downstream biological mechanisms are still poorly described. In this study, we compared the microproteomic profile of HSIL to normal tissues: ectocervix (ectoC) and endocervix (endoC). Experimental design: Tissue regions of endoC, ectoC, and HSlL were collected by laser microdissection (3500 cells each) from five patients. Samples were processed and analyzed using our recently developed laser microdissection-based microproteomic method. Tissues were compared in order to retrieve HSIL's proteomic profile. Potentially interesting proteins for pathology were stained by immunohistochemistry. Results: We identified 3072 proteins among the fifteen samples and 2386 were quantified in at least four out of the five biological replicates of at least one tissue type. We found 236 proteins more abundant in HSIL. Gene ontology enrichments revealed mechanisms of DNA replication and RNA splicing. Despite the squamous nature of HSIL, a common signature between HSIL and endoC could be found. Finally, potential new markers could support diagnosis of dysplasia in SILs. Conclusion and clinical relevance: This microproteomic investigation of HSIL gives insights into the biology of cervical precancerous lesions. © 2018 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim [less ▲]

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See detailHuman peroxidasin 1 promotes angiogenesis through ERK1/2, Akt and FAK pathways
Medfai, Hayfa; Khalil, Alia; Rousseau, Alexandre et al

in Cardiovascular Research (2019), 115(2)

The term angiogenesis refers to sprouting of new blood vessels from pre-existing ones. The angiogenic process involves cell migration and tubulogenesis requiring interaction between endothelial cells and ... [more ▼]

The term angiogenesis refers to sprouting of new blood vessels from pre-existing ones. The angiogenic process involves cell migration and tubulogenesis requiring interaction between endothelial cells and the extracellular ma- trix. Human peroxidasin 1 (hsPxd01) is a multidomain heme peroxidase found embedded in the basement mem- branes. As it promotes the stabilization of extracellular matrix, we investigated its possible role in angiogenesis both in vitro and in vivo. We analysed the effects of peroxidasin 1 gene silencing and supplementation by recombinant hsPxd01 in TeloHAEC endothelial cells on cell migration, tubulogenesis in matrigel, and intracellular signal transduction as assessed by kinase phosphorylation and expression of pro-angiogenic genes as measured by qRT–PCR. We further evaluated the angiogenic potential of recombinant peroxidasin in a chicken chorioallantoic membrane model. RNA silencing of endogenous hsPxd01 significantly reduced tube formation and cell migration, whereas supplementation by the recombinant peroxidase promoted tube formation in vitro and stimulated vascularization in vivo through its catalytic activity. Moreover, recombinant hsPxd01 promoted phosphorylation of Extracellular signal-Regulated Kinases (ERK1/2), Protein kinase B (Akt), and Focal Adhesion Kinase (FAK), and induced the expression of pro- angiogenic downstream genes: Platelet Derived Growth Factor Subunit B (PDGFB), endothelial-derived Heparin Binding EGF-like growth factor (HB-EGF), CXCL-1, Hairy-Related Transcription Factor 1 (HEY-1), DNA-binding protein inhibitor (ID-2), Snail Family Zinc Finger 1 (SNAI-1), as well as endogenous hsPxd01. However, peroxidasin silencing significantly reduced Akt and FAK phosphorylation but induced ERK1/2 activation after supplementation by recombinant hsPxd01. While hsPxd01 silencing significantly reduced expression of HEY-1, ID-2, and PDGFB, it did not affect expression of SNAI-1, HB-EGF, and CXCL-1 after supplementation by recombinant hsPxd01. Our findings suggest a role of enzymatically active peroxidasin 1 as a pro-angiogenic peroxidase and a modulator of ERK1/2, Akt and FAK signalling. [less ▲]

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See detailATG9A Is Overexpressed in Triple Negative Breast Cancer and Its In Vitro Extinction Leads to the Inhibition of Pro-Cancer Phenotypes
Claude-Taupin, Aurore; Fonderflick, Leïla; Gauthier, Thierry et al

in Cells (2018), 7(12)

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See detailHMGB1: une nouvelle cible immuno-thérapeutique
Herfs, Michael ULiege

Conference (2018, November 28)

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See detailMyoferlin controls mitochondrial structure and metabolism in pancreatic ductal adenocarcinoma, and affects tumor aggressiveness.
Rademaker, Gilles ULiege; Hennequière, Vincent; Brohée, Laura et al

Poster (2018, July 01)

Pancreatic ductal adenocarcinoma (PDAC) is the most common type of pancreatic cancer, and the third leading cause of cancer related death. Therapeutic options remain very limited and are still based on ... [more ▼]

Pancreatic ductal adenocarcinoma (PDAC) is the most common type of pancreatic cancer, and the third leading cause of cancer related death. Therapeutic options remain very limited and are still based on classical chemotherapies. Cell fraction can survive to the chemotherapy and is responsible for tumor relapse. It appears that these cells rely on oxydative phosphorylation (OXPHOS) for survival. Myoferlin, a membrane protein involved in cell fusion was recently shown by our laboratory to be overexpressed in pancreatic cancer. In the present study, we discovered that myoferlin was more expressed in cell lines undergoing (OXPHOS) than in glycolytic cell lines. In the former cell lines, we showed that myoferlin silencing reduced OXPHOS activity and forced cells to switch to glycolysis. The decrease in OXPHOS activity is associated with mitochondrial condensation and network disorganization. An increase of Dynamin-related protein (DRP)-1 phosphorylation in myoferlin-depleted cells led us to suggest mitochondrial fission, reducing cell proliferation, ATP production and inducing autophagy and ROS accumulation. Electron microscopy observation revealed mitophagy, suggesting mitochondrial alterations. To confirm the clinical importance of myoferlin in PDAC, we showed that low myoferlin expression was significantly correlated to high overall survival. Myoferlin staining of PDAC sections was negatively correlated with several 18FDG PET indices indicating that glycolytic lesions had less myoferlin. These observations are fully in accordance with our in vitro data. As the mitochondrial function was associated with cell chemoresistance, the metabolic switch induced by myoferlin silencing could open up a new perspective in the development of therapeutic strategies. Among them, targeting functional domains (C2, Dysf, …) of myoferlin should be a priority. [less ▲]

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See detailIdentification and characterization of two distinct subtypes of anal adenocarcinoma
Herfs, Michael ULiege

Conference (2018, May 31)

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See detailDeciphering the radiosensitivity of HPV-positive tumors
Bruyère, Diane ULiege; Lebeau, Alizée ULiege; RONCARATI, Patrick ULiege et al

Poster (2018, May 30)

The increased radiosensitivity of HPV positive tumors (compared to HPV negative ones) is widely known in clinical settings. However, the mechanisms by which this phenomenon occurs are still to be ... [more ▼]

The increased radiosensitivity of HPV positive tumors (compared to HPV negative ones) is widely known in clinical settings. However, the mechanisms by which this phenomenon occurs are still to be elucidated. A few hypotheses have been suggested regarding this differential radiosensitivity like, for example, an altered microtumoral environment or virus-host protein interactions. In this study, we focused on interactions between DNA repair proteins and virus oncoproteins. A large panel of 147 proteins implicated in DNA repair pathways was tested for potential interaction with HPV16 E6 and/or E7 oncoproteins using the GPCA method (Gaussia Princeps Complementation Assay). The proteins highlighted by the screening were validated by co-IP. The functional experiments, realized on HPV negative head and neck cancer (UPCI-SCC-111, FaDu, UPCI-SCC-40), vulva cancer (C33a) and control keratinocytes (HaCaT) stably transduced with E6 and/or E7, are in progress. [less ▲]

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See detailDeciphering the radiosensitivity of HPV-positive tumors
Bruyère, Diane ULiege; Lebeau, Alizée ULiege; RONCARATI, Patrick ULiege et al

Poster (2018, May 28)

The increased radiosensitivity of HPV positive tumors (compared to HPV negative ones) is widely known in clinical settings. However, the mechanisms by which this phenomenon occurs are still to be ... [more ▼]

The increased radiosensitivity of HPV positive tumors (compared to HPV negative ones) is widely known in clinical settings. However, the mechanisms by which this phenomenon occurs are still to be elucidated. A few hypotheses have been suggested regarding this differential radiosensitivity like, for example, an altered microtumoral environment or virus-host protein interactions. In this study, we focused on interactions between DNA repair proteins and virus oncoproteins. A large panel of 147 proteins implicated in DNA repair pathways was tested for potential interaction with HPV16 E6 and/or E7 oncoproteins using the GPCA method (Gaussia Princeps Complementation Assay). The proteins highlighted by the screening were validated by co-IP. The functional experiments, realized on HPV negative head and neck cancer (UPCI-SCC-111, FaDu, UPCI-SCC-40), vulva cancer (C33a) and control keratinocytes (HaCaT) stably transduced with E6 and/or E7, are in progress. [less ▲]

Detailed reference viewed: 24 (5 ULiège)