Assistant Professor
B.Sc., Rajshahi University, Bangladesh
M.Sc., Linkoping University, Sweden
Ph.D., University of Saskatchewan, Canada
Email: MSMiah@uams.edu
Office: 501-214-2455 ex 25234
UAMS Winthrop P. Rockefeller Cancer Institute
Room # 9109
Lab: 501-551-4293
Room # 9152
Research Interests
The vision of the lab is to understand how cells perceive signals that vary in healthy and cancer cells and how this perception regulates tumorigenesis and metastasis. My lab will undertake a “systemwide” interrogation of signaling networks using innovative proteomic, biochemical, and genomic techniques – to uncover how the cell decodes information within complex and combinatorial signals. We will apply these approaches to quantitatively understand healthy and cancer cell signaling in cellular decisions. For example, a long-standing biological paradox is that TGFβ signaling, which is thought to be anti-metastatic, can switch to promoting metastasis. But how the anti-metastatic function of TGFβ/SMAD signaling switches to a metastasis promoting factor is poorly understood.
Recently, we reported that breast tumor kinase (BRK), a non-receptor tyrosine kinase (nRTK), which is an oncogene and highly expressed in ~85% of human invasive ductal carcinomas, promotes metastatic potential by phosphorylating SMAD4 in mammary epithelial cells. BRK-mediated phosphorylated-SMAD4 interacts with epigenetic regulators to reprogram epigenetic gene expression in breast cancer cells. Thus, we want to (1) define the BRK regulated SMAD4 protein-interaction-network in healthy versus TNBC cells, (2) establish how phosphorylated-SMAD4 co-ordinates with chromatin remodeling complexes to alter epigenetic regulation and promote metastasis and (3) identify functionally-redundant oncogenic nRTKs for multi-target therapeutics to tackle tumorigenesis and metastasis.
The overarching goal of this research is to identify a druggable biomarker to yield a new avenue to study and treat TNBC with precision medicine therapies.