Yonsei University · 医学
Professor Seok-Gu Kang's research lab focuses on understanding the tumor microenvironment in glioblastoma (GBM), with a particular emphasis on cellular crosstalk involving mesenchymal stromal cells, immune regulation, and metabolic reprogramming. The lab investigates how signaling pathways such as C5a-p38 MAPK-ZEB1 and PD-1 immune checkpoint pathways influence GBM progression and therapy resistance. By exploring the roles of brain-resident mesenchymal stromal cells (Br-MSCs) and tumor bioenergetics, the lab aims to identify novel therapeutic targets for GBM, including metabolic and immunomodulatory strategies. Their work integrates preclinical models, flow cytometry, and transcriptomic analysis to uncover mechanisms underlying tumor invasion and immunological memory.
Figures are computed from collected data and may differ slightly.
Our findings suggest that dual inhibition of tumor bioenergetics is a novel and effective strategy for the treatment of GBM.
Our results indicate that cells similar to BM-MSCs exist in the brain. These Br-MSCs appear to be located within the vascular niche and may provide the mesenchymal elements of this niche. Because MSCs may be part of the cellular response to tissue injury, Br-MSCs may represent targets in the therapy of pathological processes such as stroke, trauma, and tumorigenesis.
Insulin exerts an anti-apoptotic activity by suppressing the excessive accumulation of ROS within cells through signaling pathways including stimulation of PI3 kinase and ERK in HepG2 cells.
<b>Background</b>: Although programmed death-1 (PD-1) blockade is effective in treating several types of cancer, the efficacy of this agent in glioblastoma (GBM) is largely unknown. <b>Methods</b>: We evaluated therapeutic effects of anti-PD-1, temozolomide (TMZ), and their combination in an orthotopic murine GBM model. The phenotype, number, and composition of lymphocytes were evaluated using flow cytometry. Transcriptional profiles of tumor tissues were analyzed using microarrays. Generation o
1. MSLCs activate p38 MAPK-ZEB1 signaling in GBM cells through C5a in a paracrine manner, thereby boosting the invasiveness of GBM cells in the tumor microenvironment.2. Neutralizing of C5a could be a potential therapeutic target for GBM by inhibition of mesenchymal phenotype.
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