Identifying the functional domains of ROR2 in regulation of of cell proliferation and migration

Details

Supervisors

Lien, Wen-Hui

Faculty

Faculté de pharmacie et des sciences biomédicales

Degree label

Master [120] en sciences biomédicales, à finalité approfondie

Abstract

The skin is the largest organs of the human body. Just like any other organs, it can develop into cancer. Skin cancer can be categorized into melanoma and non-melanoma skin cancer (NMSC). 95% of the NMSC, also termed as keratinocyte carcinoma, includes basal cell carcinoma (BCC) and cutaneous squamous cell carcinoma (cSCC). Dysregulation of several signaling pathways usually contribute to the development of these tumor types. Wnt signaling is one of commonly dysregulated signaling in cSCC. Wnt signaling can be divided into canonical and non-canonical signaling pathways. The canonical Wnt signaling pathway has been extensively studied, yet the non-canonical Wnt signaling pathway remained unclear. ROR2 is recognized as one of the non-canonical Wnt (co-)receptors and has been reported to possess a dual role, either acting as a tumor promotor or tumor suppressor, depending on cancer types. Our group has found that depletion of Ror2 in mouse skin epidermis compromised carcinogen-induced tumor formation and suppressed the progression of the skin tumor. By investigating the cellular functions of ROR2, we found that depletion of Ror2 in tumor epithelial cells reduced cell proliferation and migration. In this research thesis, we investigated the dependency of ROR2 and identified the functional domains of ROR2 in regulation of cell proliferation and migration. By conducting a loss-of-function approach in combination of protein re-repression, we discovered that STP domain of ROR2 plays a role in cell migration, but it is dispensable for ROR2-mediated cell proliferation. Our findings help us to better understand the regulatory roles of ROR2 in modulating cell proliferation and migration.