Theme：SetD2 is an epigenetic tumor suppressor and a pivotal developmental regulato

Host：Dr. Li Li

Time：28th May 2021, 16:00-17:40

Location: Room 202, Med-X Research Institute, Xuhui Campus, SJTU

Abstract: 

Significant progress has been made in our understanding of the role of epigenetic modifiers in many types of human cancer. Here, we review currently available studies on the unique histone methyltransferase, SETD2, which is responsible for H3 lysine 36 tri-methylation (H3K36me3). SETD2 plays pivotal roles in RNA alternative splicing regulation, DNA damage repair, and cytoskeleton protein methylation; inactivation of SETD2 and resultant dysregulation of these functions may lead to tumorigenesis. Despite being a newly discovered tumor suppressor, SETD2 has been found to be mutated in multiple types of cancer. Some tumors can acquire a selective growth advantage after SETD2 inactivation, which could happen in different stages in tumor progression. Decreased level of H3K36me3 caused by SETD2 inactivation has been shown to associate with higher tumor grade, tumor stage, metastasis risk, and shorter survival. Some studies also suggest that SETD2 mutation is associated with therapy resistance, therefore these SETD2-deficient tumors may need different therapeutic strategies. Moreover, deletion of SETD2 results in the developmental delay or block of mouse oocyte, sperm and early embryos. Loss of Setd2 in BMSCs in vitro facilitated differentiation propensity to adipocytes rather than to osteoblasts. Taken together, SetD2 is an epigenetic tumor suppressor and a pivotal developmental regulator.

Biography: 

Dr. Li Li is an associate professor and a PhD supervisor in School of Biomedical Engineering. He focused on the important role and mechanism of epigenetic regulatory factors in a variety of physiological and pathological processes. With histone modification as the research core, he systematically studied and elucidated the role and mechanism of epigenetic regulatory factors in diseases and development from molecular, cellular, organoid, animal and clinical data levels, which provided reliable targets and theoretical basis for clinical diagnosis and treatment of these diseases. He has published more than 30 SCI papers in Nat Genet, Cancer Cell, Nat Cell Biol, Gut, Hepatology, Nat Commun, Genes Dev, PNAS, et al, including 14 papers as first or corresponding author (IF > 130). Currently, he is the memeber of editorial board of Bosnian J basic Med and a special reviewer of Cancer Manag Res and Transl Oncol.