Eppley Institute
Assistant Professor
Molecular mechanisms and therapeutic targets of metastasis
Research Interests
Molecular targeting of
signaling molecules has the potential to be a more effective approach
for cancer treatment than those presently available. However, it has so
far had a very limited clinical impact. Thus, there remains a need for
the identification of potential cancer targets and novel approaches for
cancer treatment. One part of our research focuses on the identification
and validation of novel targets associated with cell survival, invasion
and metastasis such as gain-of-function mutation of Phosphatidylinositol
3-kinase (PI3K) and receptor tyrosine kinase Ron.
There is a fine balance between cell survival and apoptotic signalling,
which is maintained by crosstalk between oncogenes and tumor suppressors
in normal cells. However, this balance is usually broken in cancer
cells. The second part of our research focuses on the interplay of
oncogenic PI3K and Ron signaling with tumor suppressive Transforming
Growth Factor beta (TGFbeta) signaling and their role in cell survival,
invasion and metastasis. Understanding the mechanisms of metastasis will
help develop more specific and effective therapies.
Cancer stem cells have been identified in a variety of cancer types.
They are stem-like cells, have the capacity of self-renewal and have
been implicated as “tumor initiating cells”. The third part of our
research focuses on the roles of cancer stem cells in cancer metastasis
and drug resistance as well as the regulation of cancer stem cell
population by different signaling pathways that have potential role in
metastasis (i.e. PI3K, Ron, TGFbeta, etc).
We have previously identified ARK5 as a novel regulator of cellular
senescence. ARK5 is a member of AMP Activated Kinase (AMPK) family,
which is a class of Ser/Thr kinases activated by an increase in
intracellular ATP concentration. It has been demonstrated that
senescence is an intrinsic tumor suppressor mechanism that hinders
cancer progression. The fourth part of our research determines whether
ARK5 plays an essential role in oncogenic stimuli or stress-induced
premature senescence and whether inactivation of ARK5 is a putative
secondary lesion that leads to tumorigenesis in cancer.
Tel: (402) 559-5558 (Office)
E-mail: Jenny Wang