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Prominin-1, commonly known as CD133, is a pentaspan transmembrane glycoprotein that serves as a primary marker for brain tumor initiating cells (BTICs), also known as glioma stem cells (GSCs) [1]. It is localized to membrane protrusions such as microvilli and primary cilia, where it plays a role in maintaining stem cell properties and organizing the plasma membrane [2]. In the context of oncology, CD133 expression is associated with increased tumorigenicity, resistance to conventional chemotherapy and radiation, and poor prognosis in patients with glioblastoma and other high-grade gliomas [3]. Therapeutic strategies targeting CD133 include chimeric antigen receptor (CAR) T-cell therapies, monoclonal antibodies, and immunotoxins designed to selectively eliminate the stem-like population responsible for tumor recurrence [4]. However, the use of CD133 as a therapeutic target is challenged by its expression in healthy tissues, including hematopoietic stem cells and certain epithelial cells, which necessitates careful consideration of potential off-target toxicities [5]. Additionally, mutations in the PROM1 gene are linked to retinal degenerative diseases, highlighting its critical role in normal physiology [6].
Targeted elimination of CD133-positive cancer stem cells via immune-mediated lysis (e.g., CAR-T cells) or direct cytotoxicity (e.g., immunotoxins); inhibition of CD133-mediated signaling pathways such as PI3K/Akt to reduce stemness, self-renewal, and tumorigenicity.
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