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Cathepsin E (CTSE) is an intracellular aspartic protease primarily expressed in immune cells, such as macrophages and dendritic cells, and certain epithelial tissues [1]. It functions predominantly in the endosomal/lysosomal pathway, where it is involved in the processing of exogenous antigens for MHC class II presentation, thereby playing a vital role in the adaptive immune response [3]. Unlike the ubiquitously expressed Cathepsin D, Cathepsin E has a more restricted tissue distribution, which makes it an attractive target for specific therapeutic interventions [4]. In oncology, Cathepsin E mRNA and protein are significantly upregulated in pancreatic ductal adenocarcinoma and gastric cancers, often serving as a highly sensitive biomarker for early detection [2]. Its role in cancer progression involves the modulation of cell death pathways and potentially the tumor microenvironment. Therapeutic strategies targeting Cathepsin E include the development of specific protease inhibitors and the use of its enzymatic activity to activate prodrugs or imaging agents [1, 2]. Research also indicates that Cathepsin E may be involved in the pathogenesis of Alzheimer's disease and various inflammatory conditions [4]. However, its deficiency has been linked to the development of atopic dermatitis-like skin lesions, suggesting a complex role in maintaining skin homeostasis [1]. Current pharmacological interest focuses on its high specificity in certain cancer types compared to normal tissues. While no CTSE-specific drugs are currently FDA-approved, it remains a significant focus for diagnostic and targeted delivery technologies.
Inhibition of aspartic protease activity to modulate antigen presentation or tumor growth.
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