Research
Research Focus
Research Focus
In order for cells to survive environmental stresses and maintain homeostatic balance, a complex cellular signaling network integrates information about the external and internal environment in order to allow for the cells to adapt. In cancer, dysregulation of signaling disrupts the normal and well-controlled physiological homeostasis. Altered signal transduction often provides cancer cells with advantages during periods of environmental stress and enables them to grow and metastasize. Our research interest is to biochemically and molecularly decode cancer cell signaling, especially PI3K/Akt/mTOR and Ras/Raf/ERK signaling networks that are used by cancer cells to support environmental stress resistance and cancer progression.
In order for cells to survive environmental stresses and maintain homeostatic balance, a complex cellular signaling network integrates information about the external and internal environment in order to allow for the cells to adapt. In cancer, dysregulation of signaling disrupts the normal and well-controlled physiological homeostasis. Altered signal transduction often provides cancer cells with advantages during periods of environmental stress and enables them to grow and metastasize. Our research interest is to biochemically and molecularly decode cancer cell signaling, especially PI3K/Akt/mTOR and Ras/Raf/ERK signaling networks that are used by cancer cells to support environmental stress resistance and cancer progression.
Anti-cancer drug resistance mechanism and overcoming strategies
Anti-cancer drug resistance mechanism and overcoming strategies
FDA-approved targeted cancer therapy drugs are used in clinics successfully, but one of the major problems of this therapy is cancer’s resistance to the drugs. They initially lead to a dramatic decrease in tumor burden and an increase in overall patient survival. However, tumors in many patients eventually become resistant to these drugs, and tumor recurrence occurs. Thus, it is of utmost importance to determine why some cancers are resistant to targeted cancer drugs and how the resistance can be overcome for successful treatment.
FDA-approved targeted cancer therapy drugs are used in clinics successfully, but one of the major problems of this therapy is cancer’s resistance to the drugs. They initially lead to a dramatic decrease in tumor burden and an increase in overall patient survival. However, tumors in many patients eventually become resistant to these drugs, and tumor recurrence occurs. Thus, it is of utmost importance to determine why some cancers are resistant to targeted cancer drugs and how the resistance can be overcome for successful treatment.
Drugs that target mTOR and Raf/MEK signaling networks are used in clinics to treat cancer patients. Our overarching goal is to identify cancer’s resistance mechanisms toward mTOR and Raf/MEK targeting drugs and identify strategies to overcome this resistance and prevent tumor recurrence. Our discoveries will provide better approaches and strategies to determine who will benefit from or who should avoid mTOR targeting therapy, and to design effective synergistic combination therapies to overcome drug resistance.
Drugs that target mTOR and Raf/MEK signaling networks are used in clinics to treat cancer patients. Our overarching goal is to identify cancer’s resistance mechanisms toward mTOR and Raf/MEK targeting drugs and identify strategies to overcome this resistance and prevent tumor recurrence. Our discoveries will provide better approaches and strategies to determine who will benefit from or who should avoid mTOR targeting therapy, and to design effective synergistic combination therapies to overcome drug resistance.
Regulation of mRNA translation and metabolism in cancer
Regulation of mRNA translation and metabolism in cancer
With mTOR and Raf/MEK/ERK signaling networks, one of our primary focuses is on the regulation of mRNA translation, a cellular metabolic process that produces proteins. Proteins are essential parts of organisms that participate in virtually every cellular process including the structural/mechanical maintenance of cells, metabolism, immune response, muscle maintenance, and cell growth. Therefore, mRNA translation is one of the most critical processes in all living organisms, and it is tightly controlled by growth factors, hormones, and diet. The main characteristic of cancer is an uncontrolled growth and cell division, which means cancer cells require high amounts of protein production. To meet this requirement, cancer cells develop hyperactive protein synthesis systems. Therefore, targeting dysregulated protein synthesis in cancer is regarded as one of the promising strategies in targeted cancer therapeutics. We focus on the mechanisms of dysregulated mRNA translation and metabolism in cancer and determine the therapeutic strategies to regulate them effectively.
With mTOR and Raf/MEK/ERK signaling networks, one of our primary focuses is on the regulation of mRNA translation, a cellular metabolic process that produces proteins. Proteins are essential parts of organisms that participate in virtually every cellular process including the structural/mechanical maintenance of cells, metabolism, immune response, muscle maintenance, and cell growth. Therefore, mRNA translation is one of the most critical processes in all living organisms, and it is tightly controlled by growth factors, hormones, and diet. The main characteristic of cancer is an uncontrolled growth and cell division, which means cancer cells require high amounts of protein production. To meet this requirement, cancer cells develop hyperactive protein synthesis systems. Therefore, targeting dysregulated protein synthesis in cancer is regarded as one of the promising strategies in targeted cancer therapeutics. We focus on the mechanisms of dysregulated mRNA translation and metabolism in cancer and determine the therapeutic strategies to regulate them effectively.
Tumor plasticity and epithelial-to-mesenchymal transition (EMT)
Tumor plasticity and epithelial-to-mesenchymal transition (EMT)
Cell plasticity is the ability of a cell to switch its identity and phenotype. Epithelial-to-mesenchymal transition (EMT) is a cell plasticity process in which epithelial cells acquire mesenchymal properties (more elongated morphology and more migratory/invasive characteristics) through genetic/epigenetic alteration. EMT plays critical roles in physiological and pathological conditions such as wound healing, tissue regeneration, fibrosis (formation of permanent scar tissue), and cancer progression and stemness. Thus, targeting EMT has been of clinical interest. We study cell plasticity in order to determine the mechanisms by which cells change their identity and properties. We believe that our study will provide a better therapeutic option for the treatment of EMT-related fatal diseases such as cancer and fibrosis.
Cell plasticity is the ability of a cell to switch its identity and phenotype. Epithelial-to-mesenchymal transition (EMT) is a cell plasticity process in which epithelial cells acquire mesenchymal properties (more elongated morphology and more migratory/invasive characteristics) through genetic/epigenetic alteration. EMT plays critical roles in physiological and pathological conditions such as wound healing, tissue regeneration, fibrosis (formation of permanent scar tissue), and cancer progression and stemness. Thus, targeting EMT has been of clinical interest. We study cell plasticity in order to determine the mechanisms by which cells change their identity and properties. We believe that our study will provide a better therapeutic option for the treatment of EMT-related fatal diseases such as cancer and fibrosis.