Events login

College of Engineering

Warning Icon This event is in the past.
March 28, 2019 | 11:00 a.m. - 12:00 p.m.
Category: Seminar
Location: Integrative Biosciences Center IBio Conference Center | Map
6135 Woodward Ave.
Detroit , MI 48202
Cost: Free
Audience: Academic Staff, Alumni, Community, Current Graduate Students, Current Undergraduate Students, Faculty, Staff

The campus community is invited to a research seminar  

Biophysical and biochemical mechanisms of cancer in the transition to metastasis

hosted by

the Department of Chemical Engineering and Materials Science


The Office of the Vice President for Research

with guest speaker, Pilhwa Lee, Ph.D.,

Research Assistant Professor, Reproduction Sciences Program,

Department of Obstetrics and Gynecology, University of Michigan


Principal Investigator, Frankel Cardiovascular Center

Michigan Medicine, University of Michigan

March 28, 2019

11 a.m. to 12 p.m.

IBio First Floor Seminar Room

The Wayne State University campus community is invited to attend a research  presentation with guest speaker, Pilhwa Lee, Ph.D. from the University of Michigan.

The presentation will be held on March 28, 2019 at 11:00 a.m. in the first floor seminar room of IBio, located at 6135 Woodward. The seminar is free and open to the entire university community. 

Dr. Lee will present, "Biophysical and biochemical mechanisms of cancer in the transition to metastasis."

Dr. Lee earned his B.S. degree in mechanical and aerospace engineering from Seoul National University, Korea, and a Ph.D. in mathematics from the Courant Institute, New York University. 


Metastasis is usually the main factor in determining a patient’s prognosis, and many cancer drugs
are developed to inhibit metastatic invasion of tumors. However, a major stumbling block is that
genotypic and proteomic variation in metastatic cells is largely heterogeneous, which suggests
that metastatic potential is not dictated by specific mutations but, rather, can be achieved in a
large number of different ways. We propose that the heterogeneous genetic and molecular-level
changes that occur during the transition to metastasis conspire to produce specific biophysical
and biochemical changes inside the cancer cells and stroma which define metastatic potential.

In the first part of the talk, we address what cell-level biophysical alterations can produce
metastasis using mathematical modeling and examine the early stages of the transition to
metastasis: the initial evasion away from the primary tumor. This model considers 4 major
factors of epithelial biophysics: cell polarity, actomyosin contractility, cell-cell adhesion, and
cell-ECM adhesion. It is possible that any or all of these processes are modified during
metastatic transition. In order to show that our model is relevant for cancer metastasis, we begin
our investigation by first validating the model against results from wound healing assays that
probed how perturbations in cell-cell adhesion and actomyosin contractility affect cancer cell
migration rates. We then develop the model within the context of a simplified picture of a tumor
and show that localized modifications of cellular biophysics can drive spontaneous migration of
cell clusters. The biophysical alterations that we identify to be necessary for evasion away from
the initial tumor are consistent with previous reports on the effect of specific proteins on
metastatic potential and provide new insight into what factors influence metastasis.

In the second part of the talk, we have reconstructed gene regulatory networks of human skin
fibroblast with external cues of biophysical and biochemical signals. The TRAnscriptional Factor
CEll ARray (TRACER) time course data from bioluminescence of 56 transcriptional activities in
live cells was plugged into parallel reconstruction of sub-networks and global network
optimization. We inferred directly activated/inhibited genes and associated networks from the
external cues determined by hydrogel stiffness and RGD peptides, respectively. These inferred
signaling pathways were validated with a priori known gene databases.

We have discovered that the external cues may function as co-stimulators or counter-stimulators
for GATA4, SMAD3/4, ETS-1, and STAT5 among others, potentially as biomarkers for
hypertrophic, fibrotic, and inflammatory phenotypes. We propose the pathways are adapted
differentially or switched according to modulated strengths of external signals.

The system identification method discovering new mechanotransduction signaling pathways is
applicable to characterizing other gene regulatory networks in developmental processes such as
stem cell differentiation in epithelial-mesenchymal interaction and transition as well as
rationalizing combination therapy for inflammation of cancer and autoimmune diseases.

We hope you can join us for this interesting seminar!  

For more information about this event, please contact Julie O'Connor at 3135775600 or