Start main content



Nov 09, 2022

PDF Seminar (2022-11-09)

Date: Wednesday, 9 November 2022

Time: 5:00 p.m. - 6:00 p.m.

Venue: Room 2 & 3, G/F, William M.W. Mong Block, 21 Sassoon Road


5:00 p.m.

Speaker: Dr. Mingxi WENG (Post-doctoral Fellow)
Primary Supervisor: Dr. Ralf JAUCH
Presentation Title: Going straight into the brain:  turning blood into neural stem cells without a detour to pluripotency
Abstract: Advances in molecular strategies to reprogram cell fates is a promising avenue to model diseases and develop personalised therapies. The fast, safe and direct generation of induced neural stem cells (iNSCs) would provide an authentic and personalised cell model for age associated neurodegenerative diseases. We establish a robust approach to reprogram multipotent iNSCs from embryonic and aged mouse fibroblasts using an engineered Sox17 (eSOX17). eSOX17 efficiently drives iNSC reprogramming while wild-type SOX2 or SOX17 fails. In the human system, eSOX17 can also reprogram human blood cells towards iNSCs. Lineage tracing shows that emerging iNSCs do not transit through a pluripotent state if POU factors are excluded. I will discuss mechanistic underpinnings of iNSC generation and distinguishing lineage from pluripotency reprogramming.


5:30 p.m. 

Speaker: Dr. Tsz Lam Matthew WONG (Post-doctoral Fellow)
Primary Supervisor: Dr. Stephanie MA
Presentation Title: Protein tyrosine kinase 7 (PTK7) promotes metastasis in hepatocellular carcinoma under SOX9 regulation and TGF-β signaling
Abstract: Metastasis is a disease condition found in most advanced hepatocellular carcinoma (HCC) patients, which drives tumor recurrence and exists without effective treatment given its complex biological features. To effectively target this molecular complexity, there is an urgent need for more detailed examination of the molecular drivers involved in metastasis and their alternative recruitment apart from normal physiology. In this study, we discovered protein tyrosine kinase 7 (PTK7) to be specifically upregulated in metastatic and advanced HCC tissues, by bioinformatic analyses using publicly available transcriptomic data and by immunohistochemistry (IHC) performed on tissue microarrays (TMA). Bioinformatic analyses and functional assays performed in HCC cell lines revealed TGF-β signaling and SOX9 to be important activators of PTK7 expression. Functionally, the enrichment of PTK7 positively correlated with metastatic potential of HCC cells in vitro and in lung metastasis models performed in immunodeficient mice. The upregulation of PTK7 was further found to recruit epithelial-mesenchymal transition (EMT) components, SLUG and ZEB1. Our study proposed PTK7 to be a novel molecule in driving metastatic HCC, particular in response to a TGF-β-activated microenvironment. The preferential expression of PTK7 resulted in previously unobserved regulatory effect on the recruitment of EMT components, establishing PTK7 as a potential determinant of specific EMT status. Therefore, our data supported the continual development of PTK7-targeted agents as an anti-metastatic therapy.    



Should you have any enquiries, please feel free to contact Miss Angela Wong at 3917 9216.