Priscilla Hwang, Ph.D.

Associate Professor, Department of Biomedical Engineering | B.S., M.S., Ph.D., Duke University VCU College of Engineering

  • Richmond VA

Dr. Hwang's research focuses on developing 3D microphysiological systems to investigate musculoskeletal pathologies and cancer progression.

Contact

VCU College of Engineering

View more experts managed by VCU College of Engineering

Spotlight

2 min

National Institutes of Health award $1.827 million for research on collective cell migration

Priscilla Hwang, Ph.D., assistant professor in the Department of Biomedical Engineering at Virginia Commonwealth University, has received a National Institutes of Health grant for $1.827 million over five years. The award from the National Institute of General Medical Sciences will support Hwang’s innovative research project “Dissecting mechanisms of collective migration” and provide mentorship for student researchers from the high school to graduate level. Collective migration, where groups of cells move together in a coordinated manner, is critical for the successful development of tissues and plays a vital role in wound healing, metastasis, and other biological processes. Dysregulation in collective migration is often linked to developmental abnormalities and disease progression. Despite its importance, the mechanics and mechanisms driving collective migration remain poorly understood. The project is organized around three primary goals: Investigate the effect of biomechanical cues to activate leader cells and directional collective migration: Understand how biomechanical signals activate leader cells to guide the migration of cell groups. Elucidate which and how leader cell mechanics are responsible for leader cell development: Identify the specific mechanical properties and behaviors that enable leader cells to emerge and lead the collective migration process. Examine the role of cell junctional forces in collective migration: Explore how the forces at cell contacts contribute to the overall migration and coordination among cells. Hwang will leverage her expertise in 3D microphysiological systems to study collective migration in dynamic, physiologically relevant environments. Her work aims to uncover the mechanisms by which leader cells sense and respond to mechanical forces in their environment, driving the collective migration of cells. “Our understanding of collective migration, especially the mechanics and mechanisms driving this phenomenon, is very limited,” Hwang said. “Our proposal will significantly accelerate our progress toward a comprehensive understanding of collective migration and lay the foundation for advancing treatment for developmental abnormalities or diseases.” The NIH grant will also expand student research and mentoring opportunities. “This Maximizing Investigators Research Award (MIRA) only goes to the most highly talented and promising investigators, and Dr. Hwang is most deserving,” said Rebecca L. Heise, Ph.D., Inez A. Caudill, Jr. Distinguished Professor and chair of the Department of Biomedical Engineering . “The award will provide support for undergraduate and predoctoral research opportunities in this important area of fundamental research that has an impact on neonatal development, cancer, and fibrotic disease.” To ensure diverse perspectives are considered throughout the project, Hwang said students from diverse populations will be recruited, including underrepresented minorities, women, and first-generation college students. “Further, we will continue to share our passion for science with the community through developing hands-on outreach activities based on our research findings,” she added.

Priscilla Hwang, Ph.D.

Social

Areas of Expertise

tumor microenvironment
intervertebral disc
microphysiological systems
cancer metastasis
collective cell migration

Education

Duke University

BS

Biomedical & Electrical Engineering

2008

Duke University

MS

Biomedical Engineering

2012

Duke University

PhD

Biomedical Engineering

2015

Affiliations

  • Associate Member, VCU Massey Cancer Center

Media Appearances

Walk to remember and inspire: Making Strides Against Breast Cancer

Fox2 News  tv

2018-10-05

The number of deaths related to breast cancer is in decline. The upcoming Making Strides Against Breast Cancer Walk is a major boost in the effort to find a cure.

The American Cancer Society funds $6 million in research grants right here in St. Louis. One of those grants helped develop tumor-on-a-chip.

Priscilla Hwang, Ph.D., is a trained biomedical engineer and a postdoctoral research fellow at Washington University. Her combined interests offer life-saving hope for breast cancer patients.

“We’re looking at how we can investigate ways to prevent cancer metastasis,” said Dr. Hwang.

View More

Selected Articles

DDR2 controls breast tumor stiffness and metastasis by regulating integrin mediated mechanotransduction in CAFs.

ELife

Bayer SV, Grither WR, Brenot A, Hwang PY, Barcus CE, Ernst M, Pence P, Walter C, Pathak A, Longmore GD.

2019-05-30

Biomechanical changes in the tumor microenvironment influence tumor progression and metastases. Collagen content and fiber organization within the tumor stroma are major contributors to biomechanical changes (e., tumor stiffness) and correlated with tumor aggressiveness and outcome. What signals and in what cells control collagen organization within the tumors, and how, is not fully understood. We show in mouse breast tumors that the action of the collagen receptor DDR2 in CAFs controls tumor stiffness by reorganizing collagen fibers specifically at the tumor-stromal boundary. These changes were associated with lung metastases. The action of DDR2 in mouse and human CAFs, and tumors in vivo, was found to influence mechanotransduction by controlling full collagen-binding integrin activation via Rap1-mediated Talin1 and Kindlin2 recruitment. The action of DDR2 in tumor CAFs is thus critical for remodeling collagen fibers at the tumor-stromal boundary to generate a physically permissive tumor microenvironment for tumor cell invasion and metastases.

View more

Randomly Distributed K14+ Breast Tumor Cells Polarize to the Leading Edge and Guide Collective Migration in Response to Chemical and Mechanical Environmental Cues.

Cancer Research

Hwang PY, Brenot A, King AC, Longmore GD, George SC.

2019-04-15

Collective cell migration is an adaptive, coordinated interactive process involving cell-cell and cell-extracellular matrix (ECM) microenvironmental interactions. A critical aspect of collective migration is the sensing and establishment of directional movement. It has been proposed that a subgroup of cells known as leader cells localize at the front edge of a collectively migrating cluster and are responsible for directing migration. However, it is unknown how and when leader cells arrive at the front edge and what environmental cues dictate leader cell development and behavior. Here, we addressed these questions by combining a microfluidic device design that mimics multiple tumor microenvironmental cues concurrently with biologically relevant primary, heterogeneous tumor cell organoids. Prior to migration, breast tumor leader cells (K14+) were present throughout a tumor organoid and migrated (polarized) to the leading edge in response to biochemical and biomechanical cues. Impairment of either CXCR4 (biochemical responsive) or the collagen receptor DDR2 (biomechanical responsive) abrogated polarization of leader cells and directed collective migration. This work demonstrates that K14+ leader cells utilize both chemical and mechanical cues from the microenvironment to polarize to the leading edge of collectively migrating tumors. SIGNIFICANCE: These findings demonstrate that pre-existing, randomly distributed leader cells within primary tumor organoids use CXCR4 and DDR2 to polarize to the leading edge and direct migration.

View more

N-cadherin is Key to Expression of the Nucleus Pulposus Cell Phenotype under Selective Substrate Culture Conditions.

Scientific Reports

Hwang PY, Jing L, Chen J, Lim FL, Tang R, Choi H, Cheung KM, Risbud MV, Gersbach CA, Guilak F, Leung VY, Setton LA.

2016-06-13

Nucleus pulposus (NP) cells of the intervertebral disc are essential for synthesizing extracellular matrix that contributes to disc health and mechanical function. NP cells have a unique morphology and molecular expression pattern derived from their notochordal origin, and reside in N-cadherin (CDH2) positive cell clusters in vivo. With disc degeneration, NP cells undergo morphologic and phenotypic changes including loss of CDH2 expression and ability to form cell clusters. Here, we investigate the role of CDH2 positive cell clusters in preserving healthy, biosynthetically active NP cells. Using a laminin-functionalized hydrogel system designed to mimic features of the native NP microenvironment, we demonstrate NP cell phenotype and morphology is preserved only when NP cells form CDH2 positive cell clusters. Knockdown (CRISPRi) or blocking CDH2 expression in vitro and in vivo results in loss of a healthy NP cell. Findings also reveal that degenerate human NP cells that are CDH2 negative can be promoted to re-express CDH2 and healthy, juvenile NP matrix synthesis patterns by promoting cell clustering for controlled microenvironment conditions. This work also identifies CDH2 interactions with β-catenin-regulated signaling as one mechanism by which CDH2-mediated cell interactions can control NP cell phenotype and biosynthesis towards maintenance of healthy intervertebral disc tissues.

View more