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Studies of postpartum mammary gland involution reveal novel pro-metastatic mechanisms

Journal of Cancer Metastasis and Treatment 2019年第2期4卷 21-38页

作者： TayIor r.WaIIace Sarah E.TaruIIo Lyndsey S.Crump traci r.lyons Department of Medicine Division of Medical OncologyUniversity of Colorado Anschutz Medical CampusAuroraCO 80045USA Young Women’s Breast Cancer Translational Program University of Colorado Anschutz Medical CampusAuroraCO 80045USA University of Colorado Cancer Center University of Colorado Anschutz Medical CampusAuroraCO 80045USA University of Colorado Gates Center for regenerative Medicine University of Colorado Anschutz Medical CampusAuroraCO 80045USA

Postpartum involution is the process by which the lactating mammary gland returns to the pre-pregnant state after weaning. Expression of tumor-promotional collagen, upregulation of matrix metalloproteinases, infiltration of M2 macrophages, and remodeling of blood and lymphatic vasculature are all characteristics shared by the involuting mammary gland and breast tumor microenvironment. The tumor promotional nature of the involuting mammary gland is perhaps best evidenced by cases of postpartum breast cancer (PPBC), or those cases diagnosed within 10 years of most recent childbirth. Women with PPBC experience more aggressive disease and higher risk of metastasis than nulliparous patients and those diagnosed outside the postpartum window. Semaphorin 7a (SEMA7A), cyclooxygenase-2 (COX-2), and collagen are all expressed in the involuting mammary gland and, together, predict for decreased metastasis free survival in breast cancer. Studies investigating the role of these proteins in involution have been important for understanding their contributions to PPBC. Postpartum involution thus represents a valuable model for the identification of novel molecular drivers of PPBC and classical cancer hallmarks. In this review, we will highlight the similarities between involution and cancer in the mammary gland, and further define the contribution of SEMA7A/COX-2/collagen interplay to postpartum involution and breast tumor progression and metastasis.

关键词： Postpartum involution postpartum breast cancer Semaphorin 7a cyclooxygenase-2 collagen metastasis

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Helicobacter pylori arginase mutant colonizes arginase Ⅱ knockout mice

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World Journal of Gastroenterology 2011年第28期17卷 3300-3309页

作者： Songhee H Kim Melanie L Langford Jean-Luc Boucher traci L Testerman David J McGee Department of Microbiology and Immunology Louisiana State University Health Sciences Center-Shreveport University of Nebraska-Lincoln School of Biological SciencesLincoln Laboratoire de Chimie et Biochimie Pharmacologiques et Toxicologiques Université Paris Descartes

AIM: To investigate the role of host and bacterial arginases in the colonization of mice by Helicobacter pylori (***).METHODS: *** produces a very powerful urease that hydrolyzes urea to carbon dioxide and ammonium,which neutralizes *** is absolutely essential to *** pathogenesis;therefore,the urea substrate must be in ample supply for urease to work *** urea substrate is most likely provided by arginase activity,which hydrolyzes L-arginine to L-ornithine and *** work has demonstrated that *** arginase is surprisingly not required for colonization of wild-type ***,another in vivo source of the critical urea substrate must *** hypothesized that the urea source was provided by host arginase Ⅱ,since this enzyme is expressed in the stomach,and *** has previously been shown to induce the expression of murine gastric arginase Ⅱ.To test this hypothesis,wild-type and arginase (rocF) mutant *** strain SS1 were inoculated into arginase Ⅱ knockout ***: Surprisingly,both the wild-type and rocF mutant bacteria still colonized arginase Ⅱ knockout ***,feeding arginase Ⅱ knockout mice the host arginase inhibitor S-(2-boronoethyl)L-cysteine (BEC),while inhibiting > 50% of the host arginase Ⅰ?activity in several tissues,did not block the ability of the rocF mutant *** to *** contrast,BEC poorly inhibited *** arginase ***: The in vivo source for the essential urea utilized by *** urease is neither bacterial arginase nor host arginase Ⅱ;instead,either residual host arginase Ⅰ?or agmatinase is probably responsible.

关键词： Arginase Helicobacter pylori S-(2-boronoethyl)-L-cysteine Urease Mice

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Gut sterilization in experimental colitis leukocyte mediated colon injury, and effects on angiogenesis/lymphangiogenesis

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Open Journal of Gastroenterology 2013年第1期3卷 12-24页

作者： Mihir Patel Justin Olinde Allison Tatum Chaitanya V. Ganta Walter E. Cromer Ankur r. Sheth Merilyn H. Jennings J. Michael Mathis traci Testerman Paul A. Jordan Kenneth Manas Christopher P. Monceaux J. Steven Alexander Department of Cellular Biology and Anatomy LSU Health Shreveport Shreveport USA Department of Gastroenterology and Hepatology LSU Health Shreveport Shreveport USA Department of Microbiology and Immunology LSU Health Shreveport Shreveport USA Department of Molecular and Cellular Physiology LSU Health Shreveport Shreveport USA

Inappropriate responses to normal commensal bacteria trigger immune activation in both inflammatory bowel disease and experimental colitis. How gut flora contribute to the pathogenesis of inflammatory bowel disease is unclear, but may involve entrapment of leukocytes and remodeling of the vascular system. Here we evaluated how the progression and tissue remodeling in experimental colitis differ in a germ- free model of mouse colitis. Four treatment groups were used: control, antibiotic-treated (ABX), dextran sulfate colitis (DSS) and DSS pre- and co-treated with antibiotics (DSS + ABX). In days 0 - 3 of the study, germ-free mice received antibiotics (vancomycin, neomycin, and metronidazole). During the next 11 days, antibiotics were continued and DSS (3%) added to “colitis” groups. Disease activity, weight, stool form and blood were monitored daily. Mice were sacrificed and tissue samples harvested. Histopathological scores in controls (0.00) and in ABX (1.0+/–0.81) were significantly (p –0). Extents of injury, inflammation and crypt damage were all improved in DSS + ABX. The Disease Activity Index score (day 11) was significantly worse in the DSS group compared to the DSS + ABX group. Stool blood and form scores were also significantly improved among these groups. Importantly, myeloper- oxidase was significantly reduced in DSS + ABX, indicating that neutrophil infiltration was blocked. Colitis was associated with an increase in blood and lymphatic vessels;both of these events were also significantly reduced by gut sterilization. Our experiment shows that clinical and histopathological severity of colitis was significantly worse in the DSS colitis group compared to the DSS + ABX group, supporting the hypothesis that development of IBD is likely to be less severe with appropriate antibiotic treatment. In particular, gut sterilization effectively reduces leuko- cyte-dependent (PMN) injury to improve outcomes and may be an important target for therapy.

关键词： Crohn’s Disease Antibiotics Myeloperoxidase Lymphatics Angiogenesis

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