Jing (Jenny) Wang
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
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
