Date: 19 April 2023 (Wednesday)
Time: 5:00 p.m. - 6:00 p.m.
Venue: Lecture Theatre 3, G/F, William M.W. Mong Block, 21 Sassoon Road
 

5:00 p.m.

Speaker: Dr. Junyi Chen (Honorary Research Associate)
Primary Supervisor: Dr. Joshua Ho
Presentation Title: Vulture: Cloud-enabled scalable mining of microbial reads in public scRNA-seq data
Abstract: The growing large-scale single-cell data have become a valuable resource to fight against global pandemic threats caused by infectious diseases. Previous researches focusing on limited pathogens are worth reviewing while existing tools lack the scalability to deal with big public data. We introduce Vulture, a scalable cloud-based pipeline that performs microbe calling for single-cell RNA sequencing data, enabling the meta-analysis of the single-cell host-microbial studies from the public domain. The cloud version of Vulture performed 200 analyses with only 20% of the cost and 60% of the time compared to the state-of-the-art methods. Its local version is also benchmarked to be 2 to 10 times faster than opponents with consistent results. We applied Vulture to detect the upregulation of chemokine receptor crosstalk with the co-infection of SARS-CoV2 and human metapneumovirus in macrophages and monocytes from a COVID-19 bronchoalveolar lavage fluid sample. It is also applied to discover potential hepatitis B virus-related copy number variations from a hepatocellular carcinoma sample. In summary, Vulture presents a scalable and economical framework to mine unknown host-microbial interactions from large-scale public scRNA-seq data.
 

5:30 p.m. 

Speaker: Dr. Lian Zhang (Post-doctoral Fellow)
Primary Supervisor: Professor Zhongjun Zhou
Presentation Title: PRMT1 reverts the immune escape of necroptotic colon cancer through RIP3 methylation
Abstract: Necroptosis plays a double-edged sword role in necroptotic cancer cell death and tumor immune escape. How cancer orchestrates necroptosis with immune escape and tumor progression remains largely unclear. We found that RIP3, the central activator of necroptosis, was methylated by PRMT1 methyltransferase at the amino acid of RIP3 R486. The methylation of RIP3 by PRMT1 inhibited the interaction of RIP3 with RIP1 to suppress RIP1-RIP3 necrosome complex, thereby blocking RIP3 phosphorylation and necroptosis activation. Moreover, the methylation-deficiency RIP3 mutant promoted necroptosis, immune escape and colon cancer progression due to increasing tumor infiltrated myeloid-derived immune suppressor cells (MDSC), while PRMT1 reverted the immune escape of RIP3 necroptotic colon cancer. Clinical patient samples analysis revealed that the protein levels of PRMT1 and RIP3^ADMA were positively correlated in cancer tissues and both of them predicted the longer patient survival. Our study provides insights into the molecular mechanism of PRMT1-mediated RIP3 methylation in the regulation of necroptosis and colon cancer immunity, as well as reveals PRMT1 and RIP3^ADMA as the valuable prognosis markers of colon cancer.

ALL ARE WELCOME

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