Extracellular Matrix in Renal Development and Cancer

Presented at: Cell Biology 2020
C.E. Credits: P.A.C.E. CE Florida CE
Speaker
  • Senior Postdoctoral Research Fellow, GOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology Children's Hospital Los Angeles
    Biography

      I received my BS in Biology from the University of California Riverside and my Doctor of Philosophy (Ph.D.) in Development, Stem Cells, and Regenerative Medicine (DSR) from the USC Keck School of Medicine. My dissertation focused on "Renal extracellular matrix bioactivity in a range of physiological states: novel insights for kidney regeneration."  As a Senior Postdoctoral Research Fellow for the past four years, I have worked on multiple topics, including the ECM characterization in the developing kidney and Wilms' Tumor, and how the ECM influences self-renewal of nephron progenitors in kidney development and cancer. I am a member of the American Society of Transplantation TRM-COP, and I am on the editorial board of the International Journal of Clinical and Experimental Medical Sciences.


    Abstract

    The extracellular matrix (ECM) is a three-dimensional structure that provides physical support for tissues/organs and biochemical/biomechanical cues for tissue morphogenesis, differentiation, and homeostasis. The continual remodeling (degradation/new synthesis) of the ECM is crucial for tissue homeostasis, development, and injury processes and contributes/regulates tumor malignancy, growth, and patient response to cancer treatment. Recent evidence shows that Wilms’ tumor (WT), pediatric cancer that accounts for 95% of the renal malignancies in children, could be considered an aberrant nephrogenesis, where nephron progenitors (NP) expressing SIX2 and CITED1  proliferate uncontrollably, hampering terminal differentiation into functional mature nephron structures. We have characterized via transcriptomic analysis and immunohistochemistry the composition of the ECM within the WT-NP and determine its role in cancer development, and identified how modulation of ECM proteins and their receptors in the NP niche might favor self-renewal vs. differentiation. We show that by altering the NP niche, we could promote NP self-renewal maintenance and hampered differentiation. Our data suggest that ECM secreted by cancerous NP promotes tumor development and growth, thus targeting ECM remodeling processes might be essential for the development of innovative treatment specifically designed to halt WT progression, particularly in patients with severe prognosis or recurrences.

    Learning Objectives:

    1. Identify the ECM composition in Wilms’ tumor

    2. Identify how variation in the Wilms’ tumor nephron progenitor niche may promote continuous self-renewal and hamper differentiation


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