A5101962058- PI3K/AKT/mTOR signaling in cancer
- Cancer Mechanisms and Therapy
- Immune Cell Function and Interaction
- Biochemical and Molecular Research
- Metabolism, Diabetes, and Cancer
- Cancer Immunotherapy and Biomarkers
- Autophagy in Disease and Therapy
- Polyamine Metabolism and Applications
- Synthesis and biological activity
- Cellular transport and secretion
- Calcium signaling and nucleotide metabolism
- Gastrointestinal Tumor Research and Treatment
- CAR-T cell therapy research
- Adenosine and Purinergic Signaling
- Tuberous Sclerosis Complex Research
- High Altitude and Hypoxia
- CRISPR and Genetic Engineering
- Cancer Research and Treatments
- HIV/AIDS drug development and treatment
- Cancer Cells and Metastasis
- Protein Kinase Regulation and GTPase Signaling
- Piperaceae Chemical and Biological Studies
- Pancreatic function and diabetes
- Microtubule and mitosis dynamics
- Mitochondrial Function and Pathology
Seoul National University Hospital
2025
Genome and Company (South Korea)
2023
Harvard University
2010-2020
Weill Cornell Medicine
2020
Cornell University
2020
Seoul National University
2001
Abstract The kinase mTOR complex 1 (mTORC1) promotes cellular growth and is frequently dysregulated in cancers. In response to nutrients, mTORC1 activated on lysosomes by Rag Rheb guanosine triphosphatases (GTPases) drives biosynthetic processes. How limitations nutrients suppress activity remains poorly understood. We find that when amino acids are limited, the Rap1-GTPases confine perinuclear region reduce lysosome abundance, which suppresses signaling. Rap1 activation, independent of...
Abstract No biomarker can effectively screen for early gastric cancer (EGC). Players in the A disintegrin and metalloproteinase (ADAM)-natural killer group 2 member D (NKG2D) receptor axis may have a role that. As proof-of-concept pilot study, expression of ADAM8, ADAM9, ADAM10, ADAM12, ADAM17, major histocompatibility complex (MHC) class I chain-related sequence (MICA), ligand NKG2D, was investigated silico using The Cancer Genome Atlas (TCGA) database. Subsequently, mRNA protein levels...
Immune checkpoint inhibitor (ICI) clinically benefits cancer treatment. However, the ICI responses are only achieved in a subset of patients, and underlying mechanisms limited response remain unclear. 160 patients with non-small cell lung treated anti-programmed death protein-1 (anti-PD-1) or ligand-1 (anti-PD-L1) analyzed to understand early determinants ICI. It is observed that high levels intracellular adhesion molecule-1 (ICAM-1) tumors plasma associated prolonged survival. Further...
Despite considerable efforts, mTOR inhibitors have produced limited success in the clinic. To define vulnerabilities of mTORC1-addicted cancer cells and to find previously unknown therapeutic targets, we investigated mechanism piperlongumine, a small molecule identified chemical library screen specifically target with hyperactive mTORC1 phenotype. Sensitivity piperlongumine was dependent on its ability suppress RUVBL1/2-TTT, complex involved chromatin remodeling DNA repair. Cancer high...
8-Cl-cyclic adenosine monophosphate (8-Cl-cAMP) has been known to induce growth inhibition and differentiation in a variety of cancer cells by differential modulation protein kinase A isozymes. To understand the anticancer activity 8-Cl-cAMP further, we investigated effect on apoptosis human cells. Most tested exhibited upon treatment with 8-Cl-cAMP, albeit different sensitivity. Among them, SH-SY5Y neuroblastoma HL60 leukemic showed most extensive apoptosis. The was not reproduced other...
Supplementary Figures 1-2 from Enzastaurin, a Protein Kinase Cβ Inhibitor, Suppresses Signaling through the Ribosomal S6 and Bad Pathways Induces Apoptosis in Human Gastric Cancer Cells
Supplementary Figures 1-2 from Enzastaurin, a Protein Kinase Cβ Inhibitor, Suppresses Signaling through the Ribosomal S6 and Bad Pathways Induces Apoptosis in Human Gastric Cancer Cells
Mutations in the TSC1 or TSC2 genes are responsible for causing Tuberous Sclerosis Complex (TSC) and Lymphangioleiomyomatosis (LAM). These mutations lead to uncontrolled activation of mTOR complex 1 (mTORC1), a cellular protein kinase that regulates metabolism, autophagy cell growth. Cells with TSC1/2 require increased energy carbon sources meet their high metabolic needs To this demand, we have found activated mTORC1 uses distinct mechanisms increase glutamine consumption (glutaminolysis)...