1. Cell Volume Regulation in Epithelial Cancers

Homeostasis of cell volume is a fundamental cellular property . Alterations of cell volume and volume regulatory mechanisms participate in a wide variety of physiological and pathological cellular functions. Our research work focuses on the important role of cell volume regulation in epithelial cancers. Three parts of studies are included:

(1)Cellular and molecular mechanisms

We are using different types of cells representing the various stages of carcinogenesis to study the role of KCC isoforms in tumor cellular and molecular biology.

(2) KCC knockout mouse model

We are using the KO animal model to establish the important role of KCC 3 in angiogenesis and tumor immunity.

(3)Translational research

This translational study aims to identify novel gynecological cancer biomarkers and potential therapeutic targets through molecular analysis of cell volume regulator genes/proteins. (i.e. KCC3, KCC4 and NHE1)

Research Model of Cell Volume Regulation in Epithelial Cancers

2. The Effects of Soft Substratum on Epithelial Cancinogenesis

We previously demonstrated that soft substrate of collagen gel induced apoptosis in polarized cells, but not in transformed cells or fibroblasts. Ca 2+ signaling plays an important role in the regulation of cell response to different substrate rigidities. There is now convincing evidence that the alteration of Ca 2+ homeostasis is associated with cell survival and death. A Ca 2+ -based theory of carcinogenesis has been proposed. For example, alteration of Ca 2+ homeostasis has been demonstrated to initiate oncogenesis, which leads to cell transformation. Whether there exists any relationship between substratum properties and carcinogenesis is our interest.

3. The Role of Epidermal Growth Factor Induced Epithelial-Mesenchymal Transition in Cervical Cancer

The process of epithelial-mesenchymal transition (EMT) was highly associated with cervical cancer invasion and EGF played an important role in cervical EMT. We are interested in molecular mechanisms by which EGF downregulated E-cadherin and beta-catenin expression. Moreover, blockade of integrin alpha5 beta1 signaling significantly modulated EGF-mediated EMT. Unraveling the process of EMT could provide valuable information on cervical cancer malignancy.