I received a PhD degree from Mississippi State University in 1994 and then performed postdoctoral training at Johns Hopkins University School of Medicine and Scripps Research Institute. I was recruited to West Virginia University as Assistant Professor in 2000 and promoted to Associate Professor with tenure in 2006 until 2010. I was appointed Professor at Jefferson Medical College in 2010. I have published more than 130 research papers in peer-reviewed international journals, and my papers have been cited more than 12700 times by other publications. My research projects have been funded by 14 different extramural research grants since 2001, including those from National Institutes of Health (NIH), American Cancer Society and the American Heart Association. In addition, I have served on several NIH study sections for 6 years, and served on panels for 5 other funding organizations.
There are two research fields my laboratory focuses on:
1. Mechanism of carcinogenesis induced by arsenic Arsenic is widely spread in the environment such as in soil, minerals, smoke, contaminated air and water. Epidemiologic studies show inorganic arsenic exposure induces lung, skin, liver and bladder cancers. However, the etiology and molecular mechanisms of arsenic in inducing carcinogenesis still remain to be elucidated. Arsenic also is linked to non-malignant lung diseases like bronchiectasis. Our current results show that exposure of lung epithelial cells to arsenic produced high levels of reactive oxygen species (ROS). Arsenic-induced activation leads to overexpression of several proteins that are associated with cancer development and tumor growth. In addition, arsenic suppressed expression levels of a few microRNAs resulting in inducing carcinogenesis through ROS production. I just received a new NIH R01 grant for 5 years to determine: 1) which species of ROS are induced in lung epithelial cells exposed to arsenic for regulating protein overexpression and microRNA suppression; 2) the mechanism of ROS generation in arsenic-inducing cell transformation, tumor growth and angiogenesis; and. 3) what signaling pathways are involved in the process. After we learn the biological effects of arsenic and the underlying mechanisms, we will be able to develop mechanism-based interventions to prevent carcinogenesis induced by arsenic as well as lung cancers in the future.
2. My another research interest is to investigate novel mechanisms of ovarian, breast, prostate, and lung cancer development, tumor growth and angiogenesis. Our lab has been funded by NIH in this field for 11 years, and we are working on securing new NIH grants in the near future. We initially demonstrated that the protein PI3K and its signaling play an important role in angiogenesis. Angiogenesis is required for tumorigenesis; and, its inhibition represents one of the most promising approaches in cancer therapeutic treatment as well as in certain vascular diseases. We demonstrated recently that ROS and microRNA dysregulations are new important signaling molecules in cancer development, drug resistance, tumor growth, and angiogenesis. We will study mechanisms of ROS and microRNA dysregulations in several kinds of cancers. In addition, we are interested also in identifying upstream molecules of ROS and microRNAs in regulating tumor growth and angiogenesis, and in developing new anti-cancer drugs. Finally, we hope to use nanotechnology for cancer-specific targeting of these novel pathways and for establishing therapeutic strategies for human cancers in the future.