Eppley Institute
Assistant Professor
Crosstalk of TGFbeta and PI3 kinase pathways
Research Interests
Molecular targeting of
signaling molecules has the potential to be a more effective approach
for cancer treatment than 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 and the
metastatic process such as the gain of function mutant PIK3CA encoding
the catalytic subunit of Phosphatidylinositol 3-kinase (PI3K) and the
cell surface receptor Ron kinase.
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 crosstalk of
oncogenic PI3K signalling and tumor suppressive Transforming Growth
Factor (TGF) signalling and their role in cell survival and
metastasis. Understanding the mechanisms of metastasis will help develop
more specific and effective therapies.
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 third 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