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Nam, J. H.

Publications and source records attributed to Nam, J. H..

3 recordsLinked to original sources

Nutrient availability dictates cancer metabolism-based therapeutic responses of non-oncology drugs

Metabolic deregulation is a major hallmark of cancer, therefore, interventions that modify tumor nutrient availability are considered attractive adjuvants for improving clinical outcomes for cancer patients. Much work remains, however, in clarifying how the nutritional status of each patient can affect the metabolic vulnerability of drugs and inform individual medication guidelines. Working toward the goal of oncometabolic precision medicine, we introduce CM-SLP (cancer metabolism-based synthetic lethality platform), a high-throughput screening platform that explores the metabolic vulnerability of non-oncology drugs induced by altered nutrient availability and predicts the potential synthetic lethal interactions with either hyper- or hypo-nutrient conditions. We present promising CM-SLP candidates, such as propafenone and biguanides, as representative non-oncology drugs that cooperatively enhance cytotoxicity via dysregulated metabolic pathways. Furthermore, identifying mTOR and Hippo pathways as mediators of combined propafenone/hypoglycemia or biguanides/hypoglycemia treatments, respectively, we were able to circumvent the need for dietary interventions by administering the mTOR or TEAD inhibitors to induce energy stress and cancer cell death. Together, CM-SLP represents a critical step toward integrating metabolic profiling into precision oncology, offering novel therapeutic avenues tailored to individual patient needs.

cancer biology↗

Distinct modulation of calcium-activated chloride channel TMEM16A by a novel drug-binding site

TMEM16A is a calcium-activated chloride channel with significant role in multiple cellular processes. Several TMEM16A inhibitors have been identified; however, their binding sites and inhibitory mechanisms remain unclear. Using magnolol and honokiol, the two regioisomeric inhibitors, as chemical probes, we have identified a novel drug-binding site distinct from the pore region, in TMEM16A, which is described here. With electrophysiology, unbiased molecular docking and clustering, molecular dynamics simulations, and experimental validation with mutant cycle analysis, we show that magnolol and honokiol utilize different drug-binding sites, pore and non-pore pockets. The pore blocker utilizes amino acids crucial for chloride passage, whereas the non-pore blocker allosterically modulates the pore residues to hinder ion permeation. Among 17 inhibitors tested, 11 were pore blockers and six were non-pore blockers, indicating the importance of this newly identified non-pore pocket. Our study provides insights into drug-binding mechanism in TMEM16A together with a rationale for future drug development.

physiology↗

O-GlcNAc transferase suppresses necroptosis and liver fibrosis

Over a billion people suffer from chronic liver diseases worldwide, which often leads to fibrosis and then cirrhosis. Treatments for fibrosis remain experimental, in part because no unifying mechanism has been identified that initiates liver fibrosis. Here we report that O-linked {beta}-N-acetylglucosamine (O-GlcNAc) modification protects against hepatocyte necroptosis and initiation of liver fibrosis. Decreased O-GlcNAc levels were seen in patients with liver cirrhosis and in mice with ethanol-induced liver injury. Liver-specific O-GlcNAc transferase (OGT) knockout (OGT-LKO) mice exhibited ballooning degeneration and elevated circulating alanine aminotransferase (ALT) levels at an early age and progressed to liver fibrosis and portal inflammation by 10 weeks of age. OGT-deficient hepatocytes underwent excessive necroptosis and exhibited elevated protein expression levels of receptor-interacting protein kinase 3 (RIPK3) and mixed lineage kinase domain-like (MLKL), which are key mediators of necroptosis. Furthermore, glycosylation of RIPK3 by OGT reduced RIPK3 protein stability. Taken together, these findings identify OGT as a key suppressor of hepatocyte necroptosis and OGT-LKO mice may serve as an effective spontaneous genetic model of liver fibrosis.

physiology↗