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Dr. Océane Martin
INSERM U1053, University of Bordeaux

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0 gastric cancer
0 Nrf2
0 redox
0 Helicobacter pylori
0 stem cell

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gastric cancer
Nrf2
Helicobacter pylori
stem cell

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Review
Published: 24 November 2020 in Frontiers in Cell and Developmental Biology
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Cancer is a complex disease and it is now clear that not only epithelial tumor cells play a role in carcinogenesis. The tumor microenvironment is composed of non-stromal cells, including endothelial cells, adipocytes, immune and nerve cells, and a stromal compartment composed of extracellular matrix, cancer-associated fibroblasts and mesenchymal cells. Tumorigenesis is a dynamic process with constant interactions occurring between the tumor cells and their surroundings. Even though all connections have not yet been discovered, it is now known that crosstalk between actors of the microenvironment drives cancer progression. Taking into account this complexity, it is important to develop relevant models to study carcinogenesis. Conventional 2D culture models fail to represent the entire tumor microenvironment properly and the use of animal models should be decreased with respect to the 3Rs rule. To this aim,in vitroorganotypic models have been significantly developed these past few years. These models have different levels of complexity and allow the study of tumor cells alone or in interaction with the microenvironment actors during the multiple stages of carcinogenesis. This review depicts recent insights into organotypic modeling of the tumor and its microenvironment all throughout cancer progression. It offers an overview of the crosstalk between epithelial cancer cells and their microenvironment during the different phases of carcinogenesis, from the early cell autonomous events to the late metastatic stages. The advantages of 3D over classical 2D orin vivomodels are presented as well as the most promising organotypic models. A particular focus is made on organotypic models used for studying cancer progression, from the less complex spheroids to the more sophisticated body-on-a-chip. Last but not least, we address the potential benefits of these models in personalized medicine which is undoubtedly a domain paving the path to new hopes in terms of cancer care and cure.

ACS Style

Maria M. Haykal; Clara Nahmias; Christine Varon; Océane C. B. Martin. Organotypic Modeling of the Tumor Landscape. Frontiers in Cell and Developmental Biology 2020, 8, 1 .

AMA Style

Maria M. Haykal, Clara Nahmias, Christine Varon, Océane C. B. Martin. Organotypic Modeling of the Tumor Landscape. Frontiers in Cell and Developmental Biology. 2020; 8 ():1.

Chicago/Turabian Style

Maria M. Haykal; Clara Nahmias; Christine Varon; Océane C. B. Martin. 2020. "Organotypic Modeling of the Tumor Landscape." Frontiers in Cell and Developmental Biology 8, no. : 1.

Journal article
Published: 22 July 2020 in Cancers
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Cancer stem cells (CSCs) present chemo-resistance mechanisms contributing to tumour maintenance and recurrence, making their targeting of utmost importance in gastric cancer (GC) therapy. The Hippo pathway has been implicated in gastric CSC properties and was shown to be regulated by leukaemia inhibitory factor receptor (LIFR) and its ligand LIF in breast cancer. This study aimed to determine LIF’s effect on CSC properties in GC cell lines and patient-derived xenograft (PDX) cells, which remains unexplored. LIF’s treatment effect on CSC markers expression and tumoursphere formation was evaluated. The Hippo kinase inhibitor XMU-MP-1 and/or the JAK1 inhibitor Ruxolitinib were used to determine Hippo and canonical JAK/STAT pathway involvement in gastric CSCs’ response to LIF. Results indicate that LIF decreased tumorigenic and chemo-resistant CSCs, in both GC cell lines and PDX cells. In addition, LIF increased activation of LATS1/2 Hippo kinases, thereby decreasing downstream YAP/TAZ nuclear accumulation and TEAD transcriptional activity. LIF’s anti-CSC effect was reversed by XMU-MP-1 but not by Ruxolitinib treatment, highlighting the opposite effects of these two pathways downstream LIFR. In conclusion, LIF displays anti-CSC properties in GC, through Hippo kinases activation, and could in fine constitute a new CSCs-targeting strategy to help decrease relapse cases and bad prognosis in GC.

ACS Style

Lornella Seeneevassen; Julie Giraud; Silvia Molina-Castro; Elodie Sifré; Camille Tiffon; Clémentine Beauvoit; Cathy Staedel; Francis Mégraud; Philippe Lehours; Océane Martin; Hélène Boeuf; Pierre Dubus; Christine Varon. Leukaemia Inhibitory Factor (LIF) Inhibits Cancer Stem Cells Tumorigenic Properties through Hippo Kinases Activation in Gastric Cancer. Cancers 2020, 12, 2011 .

AMA Style

Lornella Seeneevassen, Julie Giraud, Silvia Molina-Castro, Elodie Sifré, Camille Tiffon, Clémentine Beauvoit, Cathy Staedel, Francis Mégraud, Philippe Lehours, Océane Martin, Hélène Boeuf, Pierre Dubus, Christine Varon. Leukaemia Inhibitory Factor (LIF) Inhibits Cancer Stem Cells Tumorigenic Properties through Hippo Kinases Activation in Gastric Cancer. Cancers. 2020; 12 (8):2011.

Chicago/Turabian Style

Lornella Seeneevassen; Julie Giraud; Silvia Molina-Castro; Elodie Sifré; Camille Tiffon; Clémentine Beauvoit; Cathy Staedel; Francis Mégraud; Philippe Lehours; Océane Martin; Hélène Boeuf; Pierre Dubus; Christine Varon. 2020. "Leukaemia Inhibitory Factor (LIF) Inhibits Cancer Stem Cells Tumorigenic Properties through Hippo Kinases Activation in Gastric Cancer." Cancers 12, no. 8: 2011.

Journal article
Published: 13 June 2020 in Cells
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Helicobacter pylori infection, the main risk factor for gastric cancer (GC), leads to an epithelial–mesenchymal transition (EMT) of gastric epithelium contributing to gastric cancer stem cell (CSC) emergence. The Hippo pathway effectors yes-associated protein (YAP) and transcriptional co-activator with PDZ binding motif (TAZ) control cancer initiation and progression in many cancers including GC. Here, we investigated the role of TAZ in the early steps of H. pylori-mediated gastric carcinogenesis. TAZ implication in EMT, invasion, and CSC-related tumorigenic properties were evaluated in three gastric epithelial cell lines infected by H. pylori. We showed that H. pylori infection increased TAZ nuclear expression and transcriptional enhancer TEA domain (TEAD) transcription factors transcriptional activity. Nuclear TAZ and zinc finger E-box-binding homeobox 1 (ZEB1) were co-overexpressed in cells harboring a mesenchymal phenotype in vitro, and in areas of regenerative hyperplasia in gastric mucosa of H. pylori-infected patients and experimentally infected mice, as well as at the invasive front of gastric carcinoma. TAZ silencing reduced ZEB1 expression and EMT phenotype, and strongly inhibited invasion and tumorsphere formation induced by H. pylori. In conclusion, TAZ activation in response to H. pylori infection contributes to H. pylori-induced EMT, invasion, and CSC-like tumorigenic properties. TAZ overexpression in H. pylori-induced pre-neoplastic lesions and in GC could therefore constitute a biomarker of early transformation in gastric carcinogenesis.

ACS Style

Camille Tiffon; Julie Giraud; Silvia Elena Molina-Castro; Sara Peru; Lornella Seeneevassen; Elodie Sifré; Cathy Staedel; Emilie Bessède; Pierre Dubus; Francis Mégraud; Philippe Lehours; Océane C.B. Martin; Christine Varon. TAZ Controls Helicobacter pylori-Induced Epithelial–Mesenchymal Transition and Cancer Stem Cell-Like Invasive and Tumorigenic Properties. Cells 2020, 9, 1 .

AMA Style

Camille Tiffon, Julie Giraud, Silvia Elena Molina-Castro, Sara Peru, Lornella Seeneevassen, Elodie Sifré, Cathy Staedel, Emilie Bessède, Pierre Dubus, Francis Mégraud, Philippe Lehours, Océane C.B. Martin, Christine Varon. TAZ Controls Helicobacter pylori-Induced Epithelial–Mesenchymal Transition and Cancer Stem Cell-Like Invasive and Tumorigenic Properties. Cells. 2020; 9 (6):1.

Chicago/Turabian Style

Camille Tiffon; Julie Giraud; Silvia Elena Molina-Castro; Sara Peru; Lornella Seeneevassen; Elodie Sifré; Cathy Staedel; Emilie Bessède; Pierre Dubus; Francis Mégraud; Philippe Lehours; Océane C.B. Martin; Christine Varon. 2020. "TAZ Controls Helicobacter pylori-Induced Epithelial–Mesenchymal Transition and Cancer Stem Cell-Like Invasive and Tumorigenic Properties." Cells 9, no. 6: 1.

Review
Published: 21 January 2020 in Toxins
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Bacterial genotoxins (BTGX) induce DNA damage, which results in senescence or apoptosis of the target cells if not properly repaired. Three BTGXs have been identified: the cytolethal distending toxin (CDT) family produced by several Gram-negative bacteria, the typhoid toxin produced by several Salmonella enterica serovars, and colibactin, a peptide-polyketide, produced mainly by the phylogenetic group B2 Escherichia coli. The cellular responses induced by BTGXs resemble those of well-characterized carcinogenic agents, and several lines of evidence indicate that bacteria carrying genotoxin genes can contribute to tumor development under specific circumstances. Given their unusual mode of action, it is still enigmatic why these effectors have been acquired by microbes and what is their role in the context of the biology of the producing bacterium, since it is unlikely that their primary purpose is to induce/promote cancer in the mammalian host. In this review, we will discuss the possibility that the DNA damage induced by BTGX modulates the host immune response, acting as immunomodulator, leading to the establishment of a suitable niche for the producing bacterium. We will further highlight open questions that remain to be solved regarding the biology of this unusual family of bacterial toxins.

ACS Style

Océane C. B. Martin; Teresa Frisan. Bacterial Genotoxin-Induced DNA Damage and Modulation of the Host Immune Microenvironment. Toxins 2020, 12, 63 .

AMA Style

Océane C. B. Martin, Teresa Frisan. Bacterial Genotoxin-Induced DNA Damage and Modulation of the Host Immune Microenvironment. Toxins. 2020; 12 (2):63.

Chicago/Turabian Style

Océane C. B. Martin; Teresa Frisan. 2020. "Bacterial Genotoxin-Induced DNA Damage and Modulation of the Host Immune Microenvironment." Toxins 12, no. 2: 63.

Journal article
Published: 26 August 2019 in Cellular Microbiology
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Several commensal and pathogenic Gram-negative bacteria produce DNA-damaging toxins that are considered bona fide carcinogenic agents. The microbiota of colorectal cancer (CRC) patients is enriched in genotoxin-producing bacteria, but their role in the pathogenesis of CRC is poorly understood. The adenomatous polyposis coli (APC) gene is mutated in familial adenomatous polyposis and in the majority of sporadic CRCs. We investigated whether the loss of APC alters the response of colonic epithelial cells to infection by Salmonella enterica, the only genotoxin-producing bacterium associated with cancer in humans. Using 2D and organotypic 3D cultures, we found that APC deficiency was associated with sustained activation of the DNA damage response, reduced capacity to repair different types of damage, including DNA breaks and oxidative damage, and failure to induce cell cycle arrest. The reduced DNA repair capacity and inability to activate adequate checkpoint responses was associated with increased genomic instability in APC-deficient cells exposed to the genotoxic bacterium. Inhibition of the checkpoint response was dependent on activation of the phosphatidylinositol 3-kinase pathway. These findings highlight the synergistic effect of the loss of APC and infection with genotoxin-producing bacteria in promoting a microenvironment conducive to malignant transformation.

ACS Style

Océane C.B. Martin; Anna Bergonzini; Federica D'Amico; Puran Chen; Jerry W. Shay; Jacques Dupuy; Mattias Svensson; Maria G. Masucci; Teresa Frisan. Infection with genotoxin‐producing Salmonella enterica synergises with loss of the tumour suppressor APC in promoting genomic instability via the PI3K pathway in colonic epithelial cells. Cellular Microbiology 2019, 21, e13099 .

AMA Style

Océane C.B. Martin, Anna Bergonzini, Federica D'Amico, Puran Chen, Jerry W. Shay, Jacques Dupuy, Mattias Svensson, Maria G. Masucci, Teresa Frisan. Infection with genotoxin‐producing Salmonella enterica synergises with loss of the tumour suppressor APC in promoting genomic instability via the PI3K pathway in colonic epithelial cells. Cellular Microbiology. 2019; 21 (12):e13099.

Chicago/Turabian Style

Océane C.B. Martin; Anna Bergonzini; Federica D'Amico; Puran Chen; Jerry W. Shay; Jacques Dupuy; Mattias Svensson; Maria G. Masucci; Teresa Frisan. 2019. "Infection with genotoxin‐producing Salmonella enterica synergises with loss of the tumour suppressor APC in promoting genomic instability via the PI3K pathway in colonic epithelial cells." Cellular Microbiology 21, no. 12: e13099.

Journal article
Published: 06 May 2019 in Microbiome
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The World Health Organization classified processed and red meat consumption as “carcinogenic” and “probably carcinogenic”, respectively, to humans. Haem iron from meat plays a role in the promotion of colorectal cancer in rodent models, in association with enhanced luminal lipoperoxidation and subsequent formation of aldehydes. Here, we investigated the short-term effects of this haem-induced lipoperoxidation on mucosal and luminal gut homeostasis including microbiome in F344 male rats fed with a haem-enriched diet (1.5 μmol/g) 14–21 days. Changes in permeability, inflammation, and genotoxicity observed in the mucosal colonic barrier correlated with luminal haem and lipoperoxidation markers. Trapping of luminal haem-induced aldehydes normalised cellular genotoxicity, permeability, and ROS formation on a colon epithelial cell line. Addition of calcium carbonate (2%) to the haem-enriched diet allowed the luminal haem to be trapped in vivo and counteracted these haem-induced physiological traits. Similar covariations of faecal metabolites and bacterial taxa according to haem-induced lipoperoxidation were identified. This integrated approach provides an overview of haem-induced modulations of the main actors in the colonic barrier. All alterations were closely linked to haem-induced lipoperoxidation, which is associated with red meat-induced colorectal cancer risk.

ACS Style

Océane C. B. Martin; Maïwenn Olier; Sandrine Ellero-Simatos; Nathalie Naud; Jacques Dupuy; Laurence Huc; Sylviane Taché; Vanessa Graillot; Mathilde Leveque; Valérie Bézirard; Cécile Héliès-Toussaint; Florence Blas Y. Estrada; Valérie Tondereau; Yannick Lippi; Claire Naylies; Lindsey Peyriga; Cécile Canlet; Anne-Marie Davila; François Blachier; Laurent Ferrier; Elisa Boutet-Robinet; Françoise Guéraud; Vassilia Théodorou; Fabrice H. F. Pierre. Haem iron reshapes colonic luminal environment: impact on mucosal homeostasis and microbiome through aldehyde formation. Microbiome 2019, 7, 1 -18.

AMA Style

Océane C. B. Martin, Maïwenn Olier, Sandrine Ellero-Simatos, Nathalie Naud, Jacques Dupuy, Laurence Huc, Sylviane Taché, Vanessa Graillot, Mathilde Leveque, Valérie Bézirard, Cécile Héliès-Toussaint, Florence Blas Y. Estrada, Valérie Tondereau, Yannick Lippi, Claire Naylies, Lindsey Peyriga, Cécile Canlet, Anne-Marie Davila, François Blachier, Laurent Ferrier, Elisa Boutet-Robinet, Françoise Guéraud, Vassilia Théodorou, Fabrice H. F. Pierre. Haem iron reshapes colonic luminal environment: impact on mucosal homeostasis and microbiome through aldehyde formation. Microbiome. 2019; 7 (1):1-18.

Chicago/Turabian Style

Océane C. B. Martin; Maïwenn Olier; Sandrine Ellero-Simatos; Nathalie Naud; Jacques Dupuy; Laurence Huc; Sylviane Taché; Vanessa Graillot; Mathilde Leveque; Valérie Bézirard; Cécile Héliès-Toussaint; Florence Blas Y. Estrada; Valérie Tondereau; Yannick Lippi; Claire Naylies; Lindsey Peyriga; Cécile Canlet; Anne-Marie Davila; François Blachier; Laurent Ferrier; Elisa Boutet-Robinet; Françoise Guéraud; Vassilia Théodorou; Fabrice H. F. Pierre. 2019. "Haem iron reshapes colonic luminal environment: impact on mucosal homeostasis and microbiome through aldehyde formation." Microbiome 7, no. 1: 1-18.

Other
Published: 28 June 2018 in Cancer Prevention Research
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Red meat is probably carcinogenic to humans (WHO/IARC class 2A), in part through heme iron-induced lipoperoxidation. Here, we investigated whether red meat promotes carcinogenesis in rodents and modulates associated biomarkers in volunteers, speculating that an antioxidant marinade could suppress these effects via limitation of the heme induced lipid peroxidation. We gave marinated or non-marinated beef with various degrees of cooking to azoxymethane-initiated rats, Min mice, and human volunteers (crossover study). Mucin-depleted foci were scored in rats, adenoma in Min mice. Biomarkers of lipoperoxidation were measured in the feces and urine of rats, mice, and volunteers. The organoleptic properties of marinated meat were tested. Fresh beef increased colon carcinogenesis and lipoperoxidation in rats and mice and lipoperoxidation in humans. Without an adverse organoleptic effect on meat, marinade normalized peroxidation biomarkers in rat and mouse feces, reduced peroxidation in human feces and reduced the number of Mucin-depleted foci in rats and adenoma in female Min mice. This could lead to protective strategies to decrease the colorectal cancer burden associated with red meat consumption.

ACS Style

Océane C.B. Martin; Nathalie Naud; Sylviane Taché; Laurent Debrauwer; Sylvie Chevolleau; Jacques Dupuy; Céline Chantelauze; Denis Durand; Estelle Pujos-Guillot; Florence Blas-Y-Estrada; Christine Urbano; Gunter G.C. Kuhnle; Véronique Santé-Lhoutellier; Thierry Sayd; Didier Viala; Adeline Blot; Nathalie Meunier; Pascal Schlich; Didier Attaix; Françoise Guéraud; Valérie Scislowski; Denis Corpet; Fabrice H.F. Pierre. Targeting Colon Luminal Lipid Peroxidation Limits Colon Carcinogenesis Associated with Red Meat Consumption. Cancer Prevention Research 2018, 11, 569 -580.

AMA Style

Océane C.B. Martin, Nathalie Naud, Sylviane Taché, Laurent Debrauwer, Sylvie Chevolleau, Jacques Dupuy, Céline Chantelauze, Denis Durand, Estelle Pujos-Guillot, Florence Blas-Y-Estrada, Christine Urbano, Gunter G.C. Kuhnle, Véronique Santé-Lhoutellier, Thierry Sayd, Didier Viala, Adeline Blot, Nathalie Meunier, Pascal Schlich, Didier Attaix, Françoise Guéraud, Valérie Scislowski, Denis Corpet, Fabrice H.F. Pierre. Targeting Colon Luminal Lipid Peroxidation Limits Colon Carcinogenesis Associated with Red Meat Consumption. Cancer Prevention Research. 2018; 11 (9):569-580.

Chicago/Turabian Style

Océane C.B. Martin; Nathalie Naud; Sylviane Taché; Laurent Debrauwer; Sylvie Chevolleau; Jacques Dupuy; Céline Chantelauze; Denis Durand; Estelle Pujos-Guillot; Florence Blas-Y-Estrada; Christine Urbano; Gunter G.C. Kuhnle; Véronique Santé-Lhoutellier; Thierry Sayd; Didier Viala; Adeline Blot; Nathalie Meunier; Pascal Schlich; Didier Attaix; Françoise Guéraud; Valérie Scislowski; Denis Corpet; Fabrice H.F. Pierre. 2018. "Targeting Colon Luminal Lipid Peroxidation Limits Colon Carcinogenesis Associated with Red Meat Consumption." Cancer Prevention Research 11, no. 9: 569-580.

Journal article
Published: 01 January 2017 in Animal
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Limiting the post-weaning intake of the young rabbit is known to improve its resistance to digestive disorders, whereas a degradation of its housing hygiene is assumed to have a negative impact on its health. This study aims at providing insights into the mechanism of digestive health preservation regarding both host (growth and immune response) and its symbiotic digestive microbiota. A 2×2 factorial design from weaning (day 28) to day 64 was set up: ad libitum intake or restricted intake at 70% of ad libitum, and high v. low hygiene of housing (n=105 per group). At day 36 and day 45, 15 animals/group were subcutaneously immunized with ovalbumin (OVA) to assess their specific immune response. Blood was sampled at 36, 45, 57 and 64 days of age to determine total and anti-OVA immunoglobulin type G (IgG) and haptoglobin levels. The cecal bacterial community was explored (18 per group) by 454 pyrosequencing of genes coding for the 16S ribosomal RNA, whereas cecal pH, NH3 and volatile fatty acid (VFA) concentrations were measured to characterize fermentative activity. A 30% reduction in feed intake reduced the growth by only 17% (P<0.001), and improved the feed conversion ratio by 15% (P<0.001), whereas the degradation of hygiene conditions slightly decreased the feed intake in ad libitum fed rabbits (−3.5%, P<0.02). As poor hygiene conditions did not affect weight gain, feed conversion was improved from day 42 (P<0.05). Restricted feeding led to a lower mortality between day 28 and day 40 (P=0.047), whereas degraded hygiene conditions decreased overall morbidity (7.8% v. 16.6%; P<0.01). Both a reduced intake and low hygiene conditions of housing affected microbiota composition and especially dominant genera belonging to the Ruminococcaceae family (P<0.01). Moreover, low hygiene was associated with a higher Ruminococcaceae/Lachnospiraceae ratio (3.7 v. 2.4; P<0.05). Cecal total VFA and pH were increased (+19%; P<0.001) and decreased (−0.1 pH unit; P<0.05), respectively, in feed-restricted rabbits. Neither specific anti-OVA IgG nor haptoglobin was affected by treatments. Total IgG concentrations were the highest in animals raised in poor hygiene conditions after 8 days of restriction, but decreased after 19 days of restriction in high hygiene conditions (−2.15%; P<0.05). In conclusion, the degradation of hygiene conditions failed to induce a systematic specific and inflammatory response in rabbit, but reduced morbidity instead. Our results suggest that the microbiota composition would be a helpful source of biomarkers of digestive health.

ACS Style

Sylvie Combes; K. Massip; Océane Martin; H. Furbeyre; L. Cauquil; Geraldine Pascal; O. Bouchez; N. Le Floc’H; O. Zemb; Isabelle Oswald; T. Gidenne. Impact of feed restriction and housing hygiene conditions on specific and inflammatory immune response, the cecal bacterial community and the survival of young rabbits. Animal 2017, 11, 854 -863.

AMA Style

Sylvie Combes, K. Massip, Océane Martin, H. Furbeyre, L. Cauquil, Geraldine Pascal, O. Bouchez, N. Le Floc’H, O. Zemb, Isabelle Oswald, T. Gidenne. Impact of feed restriction and housing hygiene conditions on specific and inflammatory immune response, the cecal bacterial community and the survival of young rabbits. Animal. 2017; 11 (5):854-863.

Chicago/Turabian Style

Sylvie Combes; K. Massip; Océane Martin; H. Furbeyre; L. Cauquil; Geraldine Pascal; O. Bouchez; N. Le Floc’H; O. Zemb; Isabelle Oswald; T. Gidenne. 2017. "Impact of feed restriction and housing hygiene conditions on specific and inflammatory immune response, the cecal bacterial community and the survival of young rabbits." Animal 11, no. 5: 854-863.

Journal article
Published: 01 April 2016 in Gastroenterology
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ACS Style

Maïwenn Olier; Sandrine Ellero-Simatos; Océane Martin; Nathalie Naud; Elisa Boutet-Robinet; Vassilia Theodorou; Hervé Robert; Fabrice H. Pierre. 330 Heme-Induced Colorectal Carcinogenesis Associated With Meat Consumption: Relationship Between Fecal Microbiome, Metabolome and Luminal Heme-Induced Lipoperoxidation Activity in Rats. Gastroenterology 2016, 150, S77 -S78.

AMA Style

Maïwenn Olier, Sandrine Ellero-Simatos, Océane Martin, Nathalie Naud, Elisa Boutet-Robinet, Vassilia Theodorou, Hervé Robert, Fabrice H. Pierre. 330 Heme-Induced Colorectal Carcinogenesis Associated With Meat Consumption: Relationship Between Fecal Microbiome, Metabolome and Luminal Heme-Induced Lipoperoxidation Activity in Rats. Gastroenterology. 2016; 150 (4):S77-S78.

Chicago/Turabian Style

Maïwenn Olier; Sandrine Ellero-Simatos; Océane Martin; Nathalie Naud; Elisa Boutet-Robinet; Vassilia Theodorou; Hervé Robert; Fabrice H. Pierre. 2016. "330 Heme-Induced Colorectal Carcinogenesis Associated With Meat Consumption: Relationship Between Fecal Microbiome, Metabolome and Luminal Heme-Induced Lipoperoxidation Activity in Rats." Gastroenterology 150, no. 4: S77-S78.

Journal article
Published: 18 March 2016 in Carcinogenesis
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Epidemiological studies have associated red meat intake with risk of colorectal cancer. Experimental studies explain this positive association by the oxidative properties of heme iron released in the colon. This latter is a potent catalyst for lipid peroxidation, resulting in the neoformation of deleterious aldehydes in the fecal water of heme-fed rats. The toxicity of fecal water of heme-fed rats was associated to such lipid peroxidation. This present study demonstrated that fecal water of hemoglobin- and beef-fed rats preferentially induced apoptosis in mouse normal colon epithelial cells than in those carrying mutation on Apc (Adenomatous polyposis coli) gene, considered as preneoplastic. Highlighting the importance of lipid peroxidation and neoformation of secondary aldehydes like 4-hydroxy-2-nonenal (HNE), we optimized the depletion of carbonyl compounds in the fecal water which turned out to abolish the differential apoptosis in both cell lines. To explain the resistance of preneoplastic cells towards fecal water toxicity, we focused on Nrf2, known to be activated by aldehydes, including HNE. Fecal water activated Nrf2 in both cell lines, associated with the induction of Nrf2-target genes related to aldehydes detoxification. However, the antioxidant defense appeared to be higher in preneoplastic cells, favoring their survival, as evidenced by Nrf2 inactivation. Taken together, our results suggest that Nrf2-dependent antioxidant response was involved in the resistance of preneoplastic cells upon exposure to fecal water of hemoglobin- and beef-fed rats. This difference could explain the promoting effect of red meat and heme-enriched diet on colorectal cancer, by initiating positive selection of preneoplastic cells.

ACS Style

Reggie Surya; Cécile Héliès-Toussaint; Océane C. Martin; Thierry Gauthier; Françoise Guéraud; Sylviane Taché; Nathalie Naud; Isabelle Jouanin; Céline Chantelauze; Denys Durand; Charlotte Joly; Estelle Pujos-Guillot; Fabrice H. Pierre; Laurence Huc. Red meat and colorectal cancer: Nrf2-dependent antioxidant response contributes to the resistance of preneoplastic colon cells to fecal water of hemoglobin- and beef-fed rats. Carcinogenesis 2016, 37, 635 -645.

AMA Style

Reggie Surya, Cécile Héliès-Toussaint, Océane C. Martin, Thierry Gauthier, Françoise Guéraud, Sylviane Taché, Nathalie Naud, Isabelle Jouanin, Céline Chantelauze, Denys Durand, Charlotte Joly, Estelle Pujos-Guillot, Fabrice H. Pierre, Laurence Huc. Red meat and colorectal cancer: Nrf2-dependent antioxidant response contributes to the resistance of preneoplastic colon cells to fecal water of hemoglobin- and beef-fed rats. Carcinogenesis. 2016; 37 (6):635-645.

Chicago/Turabian Style

Reggie Surya; Cécile Héliès-Toussaint; Océane C. Martin; Thierry Gauthier; Françoise Guéraud; Sylviane Taché; Nathalie Naud; Isabelle Jouanin; Céline Chantelauze; Denys Durand; Charlotte Joly; Estelle Pujos-Guillot; Fabrice H. Pierre; Laurence Huc. 2016. "Red meat and colorectal cancer: Nrf2-dependent antioxidant response contributes to the resistance of preneoplastic colon cells to fecal water of hemoglobin- and beef-fed rats." Carcinogenesis 37, no. 6: 635-645.

Journal article
Published: 16 December 2014 in Nutrition and Cancer
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Epidemiological studies show that heme iron from red meat is associated with increased colorectal cancer risk. In carcinogen-induced-rats, a heme iron-rich diet increases the number of precancerous lesions and raises associated fecal biomarkers. Heme-induced lipoperoxidation measured by fecal thiobarbituric acid reagents (TBARs) could explain the promotion of colon carcinogenesis by heme. Using a factorial design we studied if microbiota could be involved in heme-induced carcinogenesis, by modulating peroxidation. Rats treated or not with an antibiotic cocktail were given a control or a hemoglobin-diet. Fecal bacteria were counted on agar and TBARs concentration assayed in fecal water. The suppression of microbiota by antibiotics was associated with a reduction of crypt height and proliferation and with a cecum enlargement, which are characteristics of germ-free rats. Rats given hemoglobin diets had increased fecal TBARs, which were suppressed by the antibiotic treatment. A duplicate experiment in rats given dietary hemin yielded similar results. These data show that the intestinal microbiota is involved in enhancement of lipoperoxidation by heme iron. We thus suggest that microbiota could play a role in the heme-induced promotion of colorectal carcinogenesis.

ACS Style

Océane Martin; C. Lin; N. Naud; S. Tache; Isabelle Raymond Letron; Denis Corpet; F. H. Pierre. Antibiotic Suppression of Intestinal Microbiota Reduces Heme-Induced Lipoperoxidation Associated with Colon Carcinogenesis in Rats. Nutrition and Cancer 2014, 67, 119 -125.

AMA Style

Océane Martin, C. Lin, N. Naud, S. Tache, Isabelle Raymond Letron, Denis Corpet, F. H. Pierre. Antibiotic Suppression of Intestinal Microbiota Reduces Heme-Induced Lipoperoxidation Associated with Colon Carcinogenesis in Rats. Nutrition and Cancer. 2014; 67 (1):119-125.

Chicago/Turabian Style

Océane Martin; C. Lin; N. Naud; S. Tache; Isabelle Raymond Letron; Denis Corpet; F. H. Pierre. 2014. "Antibiotic Suppression of Intestinal Microbiota Reduces Heme-Induced Lipoperoxidation Associated with Colon Carcinogenesis in Rats." Nutrition and Cancer 67, no. 1: 119-125.

Randomized controlled trial
Published: 11 September 2013 in The American Journal of Clinical Nutrition
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Background: Processed meat intake has been associated with increased colorectal cancer risk. We have shown that cured meat promotes carcinogen-induced preneoplastic lesions and increases specific biomarkers in the colon of rats.

ACS Style

Fabrice Hf Pierre; Océane Cb Martin; Raphaelle L Santarelli; Sylviane Taché; Nathalie Naud; Françoise Guéraud; Marc Audebert; Jacques Dupuy; Nathalie Meunier; Didier Attaix; Jean-Luc Vendeuvre; Sidney S Mirvish; Gunter Cg Kuhnle; Noel Cano; Denis Corpet. Calcium and α-tocopherol suppress cured-meat promotion of chemically induced colon carcinogenesis in rats and reduce associated biomarkers in human volunteers. The American Journal of Clinical Nutrition 2013, 98, 1255 -1262.

AMA Style

Fabrice Hf Pierre, Océane Cb Martin, Raphaelle L Santarelli, Sylviane Taché, Nathalie Naud, Françoise Guéraud, Marc Audebert, Jacques Dupuy, Nathalie Meunier, Didier Attaix, Jean-Luc Vendeuvre, Sidney S Mirvish, Gunter Cg Kuhnle, Noel Cano, Denis Corpet. Calcium and α-tocopherol suppress cured-meat promotion of chemically induced colon carcinogenesis in rats and reduce associated biomarkers in human volunteers. The American Journal of Clinical Nutrition. 2013; 98 (5):1255-1262.

Chicago/Turabian Style

Fabrice Hf Pierre; Océane Cb Martin; Raphaelle L Santarelli; Sylviane Taché; Nathalie Naud; Françoise Guéraud; Marc Audebert; Jacques Dupuy; Nathalie Meunier; Didier Attaix; Jean-Luc Vendeuvre; Sidney S Mirvish; Gunter Cg Kuhnle; Noel Cano; Denis Corpet. 2013. "Calcium and α-tocopherol suppress cured-meat promotion of chemically induced colon carcinogenesis in rats and reduce associated biomarkers in human volunteers." The American Journal of Clinical Nutrition 98, no. 5: 1255-1262.