演讲嘉宾

Dr. Christopher L. Antos, Associate Professor

School of Life Sciences and Technology, ShanghaiTech University, Shanghai, China

Biography: Dr. Christopher L. Antos obtained his B.S. Degrees from Indiana University in Bloomington in 1993. He then went to Freiburg, Germany on a Fulbright Scholarship and worked in the Laboratory of Dr. Rolf Kemler at the Max-Planck Institute for Immunology. In 1996, Dr. Antos started his Ph.D. work in the laboratory of Dr. Eric Olson at UT Southwestern Medical Center at Dallas. After finishing his Ph.D., he then completed his post-doctoral training in the laboratory of Dr. Christiane Nüsslein-Volhard at the Max-Planck Institute for Developmental Biology in Tübingen, Germany from 2003-2007. In 2008, Dr. Antos established his own laboratory as faculty at the DFG-Center for Regenerative Therapies Dresden of the Technische Universit?t Dresden. Dr. Antos joined ShanghaiTech University as an Associate Professor in Dec. 2016.

Topic: Regulate an Intercellular K⁺ Circuit to Scale Embryonic Fin/limb Bud Developmental Program via Intracellular Ca²⁺ Signaling

Abstract: The increase in activity of the two-pore potassium-leak channel Kcnk5b maintains allometric juvenile growth of adult zebrafish appendages. However, it remains unknown how this channel maintains allometric growth and how its bioelectric activity is regulated to scale these anatomical structures. We show the activation of Kcnk5b is sufficient to activate several genes that are part of important development programs. We provide in vivo transplantation evidence that the activation of gene transcription is cell autonomous. We also show that Kcnk5b will induce the expression of different subsets of the tested developmental genes in different cultured mammalian cell lines, which may explain how one electrophysiological stimulus can coordinately regulate the allometric growth of diverse populations of cells in the fin that use different developmental signals. We also provide evidence that the post-translational modification of serine 345 in Kcnk5b by calcineurin regulates channel activity to scale the fin. Thus, we show how an endogenous bioelectric mechanism can be regulated to promote coordinated developmental signaling to generate and scale a vertebrate appendage.

Dr. Mengchuan Wang, Associate Chief Physician

General Surgery Department, Zhujiang Hospital, Southern Medical University, Guangzhou, China

Biography: Dr. Mengchuan Wang is an associate chief physician and master tutor in Zhujiang Hospital of Southern Medical University. He is also a postdoctoral research fellow in Massachusetts General Hospital of Harvard Medical School, a member of the Oncology MDT Working Committee of Guangdong Medical Doctor Association, and a member of Guangdong Health Information Network Association (Gastrointestinal Disease Smart Application Branch). His main clinical and research work includes minimal invasive surgical therapy and immunotherapy on gastric and colorectal cancer.

Topic: Prognosis and Immune Cell Infiltration in Non-MSI-H Colorectal Cancer

Abstract: To analyze the relationship between prognosis and immune cell infiltration in non-microsatellite instability high (non-MSI-H) colorectal cancer. Non-MSI-H colorectal cancer patients were enrolled from TCGA database. Clinical characteristics correlated to overall survival (OS) and disease-free survival (DFS) were analyzed by univariate and multivariate analysis. Risk models of OS and DFS were further calculated by stepwise regression analysis. Relationship of immune cell infiltration with tumor TNM stage and OS and DFS was evaluated. Immune signaling pathways of CD4 T cells and macrophages were detected by single-cell sequencing. Differential expression genes (DEGs) were calculated and its corresponding protein expressions were assessed. Non-MSI-H colorectal cancer patients could be classified into a high risk and a low risk group with significantly different OS and DFS. Between the two groups, CD4 T cell infiltration was marked higher in the low risk group, and innate immune cell infiltration (macrophages, mast cells and NK cells) was associated with OS and DFS. Single-cell sequencing indicated that CD4 T cells were suppressive but macrophages were relatively stimulated in tumor microenvironment. CDH8 was determined to be one of the DEGs and its high protein expression was proved by immunohistochemical staining. Furthermore, CDH8 expression was correlated to CD4 T cell and macrophage infiltration as well as OS and DFS in non-MSI-H colorectal cancer patients. So, our study indicated that non-MSI-H colorectal cancer could be classified into different groups according to OS and DFS. Re-stimulating CD4 T cell function and targeting CDH8 of tumor cells might provide a new idea of immunotherapy in the future.