Bulletin of the American Physical Society
APS March Meeting 2023
Volume 68, Number 3
Las Vegas, Nevada (March 5-10)
Virtual (March 20-22); Time Zone: Pacific Time
Session Z13: Tumor-like Spheroids Embedded in Fibrous Environments and Interacting with Immune CellsInvited
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Sponsoring Units: DBIO Chair: J. Schwarz, Syracuse University Room: Room 238 |
Friday, March 10, 2023 11:30AM - 12:06PM |
Z13.00001: Vimentin intermediate filaments increases collective cell migration through extracellular matrix networks Invited Speaker: Alison E Patteson The intermediate filament protein vimentin is associated with many diseases with phenotypes of enhanced cellular migration and aggressive invasion through the extracellular matrix (ECM) of tissues, but vimentin's role in in vivo cell migration is still largely unclear. Vimentin is important for proper cellular adhesion and force generation, which are critical to cell migration; yet, the vimentin cytoskeleton also hinders the ability of cells to squeeze through small pores in ECM, resisting migration. To identify the role of vimentin in collective cell migration, we generate spheroids of wide-type and vimentin-null mouse embryonic fibroblast and embed them in a 3D collagen matrix. We find that loss of vimentin significantly impairs the ability of the spheroid to collectively expand through collagen networks and remodel the collagen network. Traction force analysis reveals that vimentin null spheroids exert less contractile force than their wild-type counterparts. In addition, we show that vimentin-containing fibroblasts increase the invasiveness of MDA-MB-231 co-culture spheroids compared to vimentin-null fibroblasts. Altogether, these results signify that vimentin plays a critical role in enhancing migratory persistence in 3D environments, a hallmark feature of diseases such as fibrosis and cancer. |
Friday, March 10, 2023 12:06PM - 12:42PM |
Z13.00002: Modeling collective interactions between embedded spheroids and collagen fibers Invited Speaker: Tao Zhang Tumor-like spheroids are in vitro, three-dimensional cellular collectives consisting of cancerous cells. Embedding these spheroids in an in vitro fibrous environment, such as a collagen network, to mimic the extracellular matrix (ECM) of a tumor provides an essential platform to quantitatively investigate the biophysical mechanisms leading to tumor invasion. To understand the complex interplay between tumor spheroids and ECM, we construct and study a three-dimensional vertex model for tumor spheroids. In such a model, the cells are represented as deformable polyhedrons with cells sharing faces such that there are no gaps between them, otherwise known as confluent. In a bulk model with periodic boundary conditions, we find a rigidity transition as a function of the target cell shape index. For a confluent cellular collective with a finite boundary, and in the presence of lateral extensile and in-plane, radial extensile deformations, we find a significant boundary-bulk effect that is one-cell layer thick. For a cellular collective now embedded in ECM, we explore how the interplay with external ECM fibers affects the morphology and rheology of the cellular collective. We also study the effect of the interplay on the structure of ECM fibers and cell invasion capability. Our study will uncover fundamental, biophysical principles that help drive collective interactions between cells and fibers as well as set the stage for emergent interactions amongst immune cells. |
Friday, March 10, 2023 12:42PM - 1:18PM |
Z13.00003: An agent-based model of the tumor microenvironment predicts hallmarks of cancer and sets the stage for model-driven experimental design of CAR T cell therapy. Invited Speaker: Neda Bagheri Computational models are essential tools that can be used to simultaneously explain and guide biological intuition. My lab employs machine learning, dynamical systems, and agent-based modeling strategies to explain biological observations and uncover fundamental principles that drive both individual cellular decisions and cell population dynamics. We are interested in the inherent multiscale nature of biology, with a specific focus on system-level dynamics that emerge from interactions of simpler individual-level modules. In this presentation, I introduce a multiscale agent-based model of a cell population that integrates subcellular signaling and metabolism, cellular level decision processes, and dynamic vascular architecture and function to interrogate regulation among heterogeneous cell agents. The modeling framework is flexible and can be used to characterize diverse cell populations. It can also be used to inform experimental design and the design of interventions to modulate emergent population level responses. |
Friday, March 10, 2023 1:18PM - 1:54PM |
Z13.00004: Infiltration of Immune Cells into Tumors; a necessary part of immunotherapy Invited Speaker: Herbert Levine The most exciting breakthroughs in cancer treatment over the last few years have involved activating the adaptive immune system to attack tumor cells. One of the key requirements of a successful attack of a solid tumor is the infiltration of cytotoxic T cells into the tumor. This talk will focus how one can use computational models to better understand the factors governing infiltration dynamics. Our ideas can be applied both to in vitro experimental systems and also directly to patient imaging data. |
Friday, March 10, 2023 1:54PM - 2:30PM |
Z13.00005: Killer immune cell swarming and solid tumor interactions Invited Speaker: Maté Biro Cytotoxic lymphocytes, also known as killer immune cells, can migrate rapidly and with striking versatility in a continuous search for cells to subdue. Adoptive cell transfer immunotherapies attempt to harness the capacity of T cells and natural killer (NK) cells to effectively locate, engage and kill cancer targets, yet they have thus far largely proved unsuccessful when targeting solid malignancies due to insufficient tumor infitration. The mechanisms and cellular forces that underpin the coordinated movements and interactions of killer immune cells and tumor cells are incompletely understood. |
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