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Dec 13, 2019

RPG Seminar Series (Speaker: Mr. CHENG Tao / Mr. YAN Dongdong)

Date: Friday, 12 December 2019

Venue: Seminar Room 1, G/F
Laboratory Block, Faculty of Medicine Building
21 Sassoon Road, Hong Kong

Time: 5:00 p.m.

Title: The function of chromatin architectural protein CTCF in HBV transcription
Speaker: Mr. CHENG Tao (PhD candidate)

Chromatin architectural protein CTCF is a multifunctional protein, repressing gene expression or activating gene expression, which depends on the interaction with other proteins. Currently, it is unknown about the role of CTCF in HBV transcription. In my study, knocking down CTCF inhibits HBV transcription, while overexpression of CTCF promotes HBV gene expression, indicating that CTCF have a positive effect on HBV transcription. Our results of ChIP assay also show that there are the CTCF binding sites in HBV genome, and CTCF can affect the histone modifications of HBV genome. We will fine map the sequences of the CTCF binding sites, and will investigate the mechanism by which CTCF promotes HBV transcriptions.

Title: Roles and mechanisms of serglycin in the tumor microenvironment of esophageal cancer
Speaker: Mr. YAN Dongdong (PhD candidate)

Serglycin, an intracellular and secretory proteoglycan, has been reported to be associated with malignant cancer progression. However, its role in esophageal squamous cell carcinoma (ESCC) remains elusive. Our recent data showed that serglycin was overexpressed in ESCC and lymph node metastasis, and that its overexpression can enhance the invasion of ESCC cells. Here, we explore the effects and mechanisms of serglycin in the tumor microenvironment. We found that the chemokine and cytokine profiles, and the exosomal contents in the conditioned medium of ESCC cells were altered after serglycin overexpression. Midkine, a heparin-binding growth factor, was upregulated. Our results showed that exogenous midkine activated esophageal fibroblasts and increased their migration ability. Furthermore, exosomes derived from serglycin-overexpressing ESCC cells could enhance the invasion and the tube formation ability of human umbilical vein endothelial cells. All these effects suggest that serglycin can create a pro-cancerous microenvironment via altering the ESCC cell secretome.