Date: 29 February 2024 (Thursday)
Time: 5:00 pm – 6:00 pm
Venue: Cheung Kung Hai Lecture Theatre 1, G/F, William M.W. Mong Block, 21 Sassoon Road
 

5:00 p.m.

Presenter: Mengya Xu (PhD candidate)
Primary Supervisor: Prof. Michael HUEN
Presentation Title: Role of ZC3H8 in response to DSB on nucleolar chromatin
Abstract: The nucleolus represents the site of ribosomal RNA (rRNA) synthesis and has evolved to couple ribosome biogenesis with stress detection and response. Indeed, it is now established that the nucleolus is a central hub that coordinates diverse biological processes, including cell cycle progression and DNA repair (1, 2). The nucleolus represents a highly specialized domain that is a challenge for the cell to maintain and sustain in the context of DNA damage signaling and repair. However, how the nucleolus integrates signals and responds to DNA damage is only beginning to be unraveled.

In this study, we identified Zinc Finger protein ZC3H8 as a DNA damage respondent with a nucleolar-specific role. Our findings support the idea that the nucleolus serves as a stress sensor and by regulating protein shuttling across the nuclear sub-compartments, plays key roles in response to DNA damage.

5:30 p.m.

Presenter: Ut Kei LOU (PhD candidate)
Primary Supervisor: Prof. Stephanie MA
Presentation Title: Microtubule-associated protein MAP2 promotes drug resistance and cancer stemness in hepatocellular carcinoma through integrin dysregulation
Abstract: Integrins mediate cell adhesion and transmission of mechanical and chemical signals. Dysregulated integrin signaling empowers tumor cells with abilities to drive cancer stem cell functions, including tumor initiation, epithelial plasticity, and resistance to therapies. Hepatocellular carcinoma (HCC) cells marked by CD133 represent an important functional subset displaying a dedifferentiated status with stem cell traits. In this study, transcriptome profiling of ‘normal’ CD133+ cells isolated from regenerating liver against ‘HCC’ CD133+ cells isolated from NRAS+AKT-driven HCC revealed downregulation of integrin α family. One of the most upregulated genes, MAP2, demonstrated the ability to suppress integrin expression. Functionally, MAP2 promoted tumor initiation and conferred resistance to sorafenib. Pharmacological inhibition of MAP2 attained a synergistic effect with sorafenib in suppressing growth of HCC cell lines, patient-derived organoids and mice model. On-going research is focused on the study of MAP2 regulation on integrin signaling in the maintenance of a more stemness state in HCC.

ALL ARE WELCOME

Should you have any enquiries, please feel free to contact Jerry Siu at 3917 6912.