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Pancreatic Cancer Invasion of the Lymphatic Vasculature and Contributions of the Tumor Microenvironment: Roles for E- Selectin and CXCR4

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Pancreatic Cancer Invasion of the Lymphatic Vasculature and Contributions of the Tumor Microenvironment: Roles for E- Selectin and CXCR4 University of Nebraska Medical Center DigitalCommons@UNMC Theses & Dissertations Graduate Studies Fall 12-16-2016 Pancreatic Cancer Invasion of the Lymphatic Vasculature and Contributions of the Tumor Microenvironment: Roles for E- selectin and CXCR4 Maria M. Steele University of Nebraska Medical Center Follow this and additional works at: https://digitalcommons.unmc.edu/etd Recommended Citation Steele, Maria M., "Pancreatic Cancer Invasion of the Lymphatic Vasculature and Contributions of the Tumor Microenvironment: Roles for E-selectin and CXCR4" (2016). Theses & Dissertations. 166. https://digitalcommons.unmc.edu/etd/166 This Dissertation is brought to you for free and open access by the Graduate Studies at DigitalCommons@UNMC. It has been accepted for inclusion in Theses & Dissertations by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. i PANCREATIC CANCER INVASION OF THE LYMPHATIC VASCULATURE AND CONTRIBUTIONS OF THE TUMOR MICROENVIRONMENT: ROLES FOR E-SELECTIN AND CXCR4 By Maria M. Steele A DISSERTATION Presented to the Faculty of the University of Nebraska Graduate College in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy Cancer Research Graduate Program Under the Supervision of Professor Michael A. Hollingsworth University of Nebraska Medical Center Omaha, NE November, 2016 Supervisory Committee Michael A. Hollingsworth, Ph.D. Kaustubh Datta, Ph.D. Angie Rizzino, Ph.D. Joyce C. Solheim, Ph.D. ii PANCREATIC CANCER INVASION OF THE LYMPHATIC VASCULATURE AND CONTRIBUTIONS OF THE TUMOR MICROENVIRONMENT: ROLES FOR E-SELECTIN AND CXCR4 Maria M. Steele University of Nebraska, 2016 Advisor: Michael A. Hollingsworth ABSTRACT As the fourth leading cause of cancer-related deaths, pancreatic cancer is one of the most lethal forms of cancers in the United States. Lymphatic vessel invasion and subsequent metastasis to the lymph nodes are early and significant events observed during pancreatic cancer progression and are used to determine patient prognosis and therapy selection. Although clinicians and researchers recognize the importance of lymph node involvement for patient prognosis and therapy selection, the biological mechanisms that govern lymphatic invasion and metastasis and the contributions of the pancreatic tumor microenvironment to these processes remain poorly understood. In this dissertation, we characterize the interactions of lymphatic endothelial cells with pancreatic tumor cells and pancreatic fibroblasts, showing that while both cell types accelerate lymphangiogenesis, pancreatic fibroblasts are the major recruiters of lymphatic endothelial cells. Additionally, we evaluated pancreatic tumor cell invasion of lymphatics and demonstrated that adhesion protein E-selectin regulates pancreatic tumor adhesion to and transendothelial migration across a lymphatic endothelium. Blockade of E-selectin using a novel glycomimetic inhibitor, GMI-1271, significantly impaired these processes if pancreatic tumor cells expressed the proper E-selectin ligands. E-selectin blockade in vivo significantly impaired pancreatic tumor metastasis to a number of organs sites including the lymph nodes. This iii impairment of metastasis through the lymphatic vasculature by GMI-1271 was not due to changes in lymphatic vessel density, but rather tumor cell interactions with the lymphatic endothelium. Chemokine receptor CXCR4 and its ligand CXCL12 have also been implicated in facilitating pancreatic tumor progression and metastasis. Using a novel small molecule inhibitor of both CXCR4 and E-selectin, we demonstrated that CXCR4 blockade significantly impairs pancreatic tumor cell adhesion and transendothelial migration across a lymphatic endothelium independent of tumor cell expression of E-selectin ligands. In vivo blockade of both CXCR4 and E-selectin moderately impaired pancreatic tumor metastasis. However, this inhibition of metastasis through GMI-1359 administration did not prolong animal survival even when administered in combination with chemotherapy and immunotherapy. Examination of pancreatic tumor microenvironment following GMI-1359 treatment revealed significant changes to the cell cellular composition: drastically reduced desmoplasia and lymphatic vascular densities. Further studies are ongoing to evaluate GMI-1359 efficacy in combination with immunotherapy in spontaneous mouse models of pancreatic cancer. Altogether, our data demonstrates that lymphatic biology and function is affected by both pancreatic tumor cells and pancreatic fibroblasts, and that factors expressed by the lymphatic endothelium ((E-selectin and CXCR4) may be targetable for the treatment of pancreatic cancer. iv ACKNOWLEDGEMENTS Firstly, I would like to acknowledge my advisor, Dr. Tony Hollingsworth. I think the single most important lesson I learned under your mentorship is how to step back and examine the big picture. Early during my graduate studies, I spent a lot of time focused on very specific mechanisms within pancreatic cancer. However, you challenged me to evaluate how a single mechanism impacts the whole disease including the tumor, the local tumor microenvironment, and the distant metastatic microenvironment, resulting in novel and exciting questions regarding pancreatic cancer. I am a better scientist because of this. Also, thank you for all your time and efforts in teaching me the skills necessary to pursue a career in science: critical thinking, experimental design, scientific writing, and much more. I have had many unique opportunities since joining your laboratory such as participating in the rapid autopsy program, collaborating with a drug company, learning live cell imaging, and developing various in vivo experiments. For these opportunities and your mentorship, I am very grateful. I would also like to acknowledge my supervisory committee members, Drs. Kaustubh Datta, Angie Rizzino, and Joyce Solheim. Thank you for all your wonderful ideas, advice, and support through the years. Each of you has unique mentorship styles which has enabled me to evaluate problems from different perspectives and made me a more well-rounded scientist. Over the years, I have had the opportunity to work with many talented individuals within the Hollingsworth laboratory. I thank all of my labmates for being so generous with their time in helping me with my studies. In particular, all the in vivo studies would not have been possible without all of your help and for that I am truly grateful. Also, thank you for all of your insights and troubleshooting suggestions over the years: you are all so very knowledgeable and I have learned so much from my discussions with each of you. Thank you for being such wonderful colleagues. Dr. Jim Grunkemeyer and Kelly O’Connell – thank you for all your help in the v process of imaging mice and administering treatments when I was unavailable. The drug trial studies would have come to a standstill if not for your help. I would also like to specially acknowledge Dr. Darci Fink. As a talented scientist, your studies on lymphatic biology were an invaluable resource for my own work. Moreover, thank you for working with me to assemble a comprehensive review of the role of lymphatics in pancreatic cancer - that work would not have been possible without your help. I would also like to thank Dr. Erin Wuebben for all of her insight and support. You are a fantastic scientist and an even better friend. Thank you so much for helping me to survive graduate school! I would like to thank my family for all their encouragement. To my parents, especially, you have both always provided me with unyielding support and encouragement. I am a determined and hardworking person because you both were fantastic examples of these qualities. You never let me quit anything and always encouraged me to put in the hard work necessary to get through graduate school and life. Your love and support means the world to me. Thank you. Additionally, to all my siblings – Michael, Tim, Joe, Sam, and Becky – thank you for keeping life fun and exciting. Graduate school was not such an arduous process with all of you around. Lastly, I would like to acknowledge my husband, Mark. Thank you for encouraging me to pursue a career in science. I know these past few years have been as hard on you as they have been on me. When I was frustrated and felt like a failure, you picked me up then made me laugh; I am so grateful that you have been there to support me. Your own intelligence keeps me on my toes and challenges me to learn new things. I would not be the scientist or person I am today without you. Thank you for all your love and support. vi TABLE OF CONTENTS ABSTRACT ..................................................................................................................................... ii ACKNOWLEDGEMENTS ............................................................................................................ iv TABLE OF CONTENTS ................................................................................................................ vi LIST OF FIGURES ......................................................................................................................... x LIST OF TABLES ........................................................................................................................ xiv ABBREVIATIONS ....................................................................................................................... xv CHAPTER 1: ..................................................................................................................................
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