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6. Antibody-Drug Conjugates in Urothelial Cancer: From Scientific Rationale to Clinical Development.

Author

Kwon, Whi-An, Lee, Seo-Yeon, Jeong, Tae Yoong, Kim, Hyeon Hoe, and Lee, Min-Kyung

Subjects
*DRUG toxicity, *IMMUNOGLOBULINS, *DRUG efficacy, *DISEASE progression, *DRUG resistance, BLADDER tumors
Abstract

Simple Summary: For metastatic urothelial cancer (UC), platinum-based chemotherapy and immunotherapy are used, with newer treatments like monoclonal antibodies (e.g., pembrolizumab) showing varied success. Traditional treatments often fail to provide long-term responses. Advances in molecular understanding of UC have led to targeted therapies, identifying six UC subclasses influencing treatment responses. Promising drugs include the fibroblast growth factor receptor inhibitor erdafitinib and antibody-drug conjugates (ADCs). ADCs represent a significant advancement in UC treatment, using monoclonal antibodies linked to cytotoxic agents to target cancer cells. UC is suitable for ADC therapy due to high antigen expression, enhancing efficacy while reducing systemic toxicity. Despite immune checkpoint inhibitors, advanced UC progresses rapidly with poor survival rates. Notable ADCs include enfortumab vedotin, effective alone and with pembrolizumab, and sacituzumab govitecan, showing effectiveness in studies. This review covers ADC mechanisms, mono- and combination therapies, resistance, and future perspectives, highlighting ADCs' vital role in treating UC. Antibody-drug conjugates (ADCs) have been a significant advancement in cancer therapy, particularly for urothelial cancer (UC). These innovative treatments, originally developed for hematological malignancies, use target-specific monoclonal antibodies linked to potent cytotoxic agents. This rational drug design efficiently delivers cancer cell-killing agents to cells expressing specific surface proteins, which are abundant in UC owing to their high antigen expression. UC is an ideal candidate for ADC therapy, as it enhances on-target efficacy while mitigating systemic toxicity. In recent years, considerable progress has been made in understanding the biology and mechanisms of tumor progression in UC. However, despite the introduction of immune checkpoint inhibitors, advanced UC is characterized by rapid progression and poor survival rates. Targeted therapies that have been developed include the anti-nectin 4 ADC enfortumab vedotin and the fibroblast growth factor receptor inhibitor erdafitinib. Enfortumab vedotin has shown efficacy in prospective studies in patients with advanced UC, alone and in combination with pembrolizumab. The anti-Trop-2 ADC sacituzumab govitecan has also demonstrated effectiveness in single-armed studies. This review highlights the mechanism of action of ADCs, their application in mono- and combination therapies, primary mechanisms of resistance, and future perspectives for their clinical use in UC treatment. ADCs have proven to be an increasingly vital component of the therapeutic landscape for urothelial carcinoma, filling a gap in the treatment of this progressive disease. [ABSTRACT FROM AUTHOR]

Published
2024
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12. LSR/angulin-1 is a tricellular tight junction protein involved in blood–brain barrier formation

Author

Sohet, Fabien, Lin, Christina, Munji, Roeben N, Lee, Seo Yeon, Ruderisch, Nadine, Soung, Allison, Arnold, Thomas D, Derugin, Nikita, Vexler, Zinaida S, Yen, Frances T, and Daneman, Richard

Subjects
Neurosciences, Autoimmune Disease, Multiple Sclerosis, Stroke, Neurodegenerative, Brain Disorders, Underpinning research, 1.1 Normal biological development and functioning, Neurological, Animals, Blood-Brain Barrier, Brain, Cell Line, Encephalomyelitis, Autoimmune, Experimental, Female, Infarction, Middle Cerebral Artery, Mice, Inbred C57BL, Mice, Knockout, Receptors, Lipoprotein, Tight Junctions, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

The blood-brain barrier (BBB) is a term used to describe the unique properties of central nervous system (CNS) blood vessels. One important BBB property is the formation of a paracellular barrier made by tight junctions (TJs) between CNS endothelial cells (ECs). Here, we show that Lipolysis-stimulated lipoprotein receptor (LSR), a component of paracellular junctions at points in which three cell membranes meet, is greatly enriched in CNS ECs compared with ECs in other nonneural tissues. We demonstrate that LSR is specifically expressed at tricellular junctions and that its expression correlates with the onset of BBB formation during embryogenesis. We further demonstrate that the BBB does not seal during embryogenesis in Lsr knockout mice with a leakage to small molecules. Finally, in mouse models in which BBB was disrupted, including an experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis and a middle cerebral artery occlusion (MCAO) model of stroke, LSR was down-regulated, linking loss of LSR and pathological BBB leakage.

Published
2015

16. SH003 Causes ER Stress-mediated Apoptosis of Breast Cancer CellsviaIntracellular ROS Production

Author

LEE, SEO YEON, KIM, TAE HOON, CHOI, WON GEUN, CHUNG, YOON HEY, KO, SEONG-GYU, CHEON, CHUNHOO, and CHO, SUNG-GOOK

Subjects
Cancer Research, Cell Line, Tumor, Genetics, Humans, Female, Breast Neoplasms, Apoptosis, Antineoplastic Agents, Angiogenesis Inhibitors, Reactive Oxygen Species, Molecular Biology, Biochemistry, Research Article
Abstract

Background/Aim: Breast cancer is one of the most common cancers in women all over the world and new treatment options are urgent. ER stress in cancer cells results in apoptotic cell death, and it is being proposed as a new therapeutic target. SH003, a newly developed herbal medicine, has been reported to have anti-cancer effects. However, its molecular mechanism is not yet clearly defined. Materials and Methods: Microarray was performed to check the differential gene expression patterns in various breast cancer cell lines. Cell viability was measured by MTT assays to detect cytotoxic effects. Annexin V-FITC and 7AAD staining, TUNEL assay and DCF-DA staining were analyzed by flow cytometry to evaluate apoptosis and ROS levels, respectively. Protein expression was examined in SH003-breast cancer cells using immunoblotting assays. The expression of C/EBP Homologous Protein (CHOP) mRNA was measured by real-time PCR. The effects of CHOP by SH003 treatment were investigated using transfection method. Results: Herein, we investigated the molecular mechanisms through which SH003 causes apoptosis of human breast cancer cells. Both cell viability and apoptosis assays confirmed the SH003-induced apoptosis of breast cancer cells. Meanwhile, SH003 altered the expression patterns of several genes in a variety of breast cancer cell lines. More specifically, it upregulated gene sets including the response to unfolded proteins, independently of the breast cancer cell subtype. In addition, SH003-induced apoptosis was due to an increase in ROS production and an activation of the ER stress-signaling pathway. Moreover, CHOP gene silencing blocked SH003-induced apoptosis. Conclusion: SH003 causes apoptosis of breast cancer cells by upregulating ROS production and activating the ER stress-mediated pathway. Thus, our findings suggest that SH003 can be a potential therapeutic agent for breast cancer.

Published
2022

17. Severity of polycystic kidney disease revealed by multiparametric MRI

Author

Wang, Feng, primary, Lee, Seo Yeon, additional, Adelnia, Fatemeh, additional, Takahashi, Keiko, additional, Harkins, Kevin D., additional, He, Lilly, additional, Zu, Zhongliang, additional, Ellinger, Philipp, additional, Grundmann, Manuel, additional, Harris, Raymond C., additional, Takahashi, Takamune, additional, and Gore, John C., additional

Published
2023
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