Jan 10, 2020
RPG Seminar Series (Speaker: Miss YU Wing Shan / Miss HU Feng)
Date: Friday, 10 January 2020
Venue: Seminar Room 4, G/F
Laboratory Block, Faculty of Medicine Building
21 Sassoon Road, Hong Kong
Time: 5:00 p.m.
Title: Transcorneal electrical stimulation induced antidepressant-like effects in rat models
Speaker: Miss YU Wing Shan (PhD candidate)
Transcorneal electrical stimulation (TES) is a non-invasive therapy in ophthalmological diseases. Evidence suggests that visual impairment is highly correlated with depression. Although TES is shown to improve visual functions, the effects of TES on neuropsychiatric diseases remain unclear. In this study, although histological study shows that TES did not rescue the degenerating photoreceptors in the transgenic rats, we found that TES treatment exerted antidepressant-like activities in the S334ter-line-3 rat model of retinal degeneration. The effects of TES were further validated in a rat model of depression using the chronic unpredictable stress paradigm. Similarly, rats with TES treatment showed a decrease in depressive-like behaviors. These results were further supported by the gene expression study showing the upregulation of neurogenesis-related genes in the hippocampus. Taken together, our study suggested that TES could be a potential therapy for depression.
Title: Elucidating the mechanistic role of DEPDC1B in promoting melanoma metastasis
Speaker: Miss HU Feng (PhD candidate)
Melanoma is responsible for most skin cancer deaths because of its highly metastatic behaviour. Current ineffective therapeutic regimen management prompts us to identify new druggable targets in governing the systemic spread of melanoma. DEPDC1B has been shown to function as an oncogene in several cancer contexts, yet its roles in melanoma are not fully revealed. Here we found high expression of DEPDC1B in melanoma was associated with poor survival that coincided with its oncogenic roles in in promoting melanoma growth and invasion in vitro. In addition, Rac1 activation assay demonstrated that DEPDC1B knockdown resulted in decreased levels of active Rac1 and subtle elevation of active RhoA which is known to act in an antagonistic manner to Rac1 in governing cell invasion. Thus, the results obtained so far suggest that DEPDC1B could promote melanoma metastasis possibly through the regulation of Rac1 activity and its underlying mechanisms remain to be elucidated.
ALL ARE WELCOME