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Palladin is a critical cytoskeletal scaffolding protein encoded by the PALLD gene that plays a fundamental role in organizing the actin cytoskeleton, thereby influencing cell shape, motility, and adhesion [1, 2]. It is ubiquitously expressed in mesenchymal tissues and localizes to actin-rich structures such as stress fibers, focal adhesions, and invadopodia [4, 7]. In the context of oncology, palladin is significantly overexpressed in the tumor stroma, particularly within cancer-associated fibroblasts (CAFs) of pancreatic ductal adenocarcinoma, where it promotes a pro-invasive environment and facilitates metastasis [3, 30]. Mutations in the PALLD gene have also been linked to familial pancreatic cancer susceptibility [8, 10]. As a therapeutic target, research focuses on downregulating palladin mRNA using RNA interference (siRNA/shRNA) or microRNAs (such as miR-96 and miR-182) to inhibit cancer cell invasion and normalize the tumor microenvironment [7, 31]. While no drugs targeting palladin are currently approved for clinical use, experimental antisense oligonucleotides and siRNA-based approaches have demonstrated efficacy in reducing tumor progression and metastasis in preclinical models [26, 28]. Additionally, palladin expression serves as a potent biomarker for disease progression and poor prognosis in various malignancies, including glioma and renal cell carcinoma [24, 34].
RNA interference (siRNA/shRNA), microRNA-mediated downregulation, antisense inhibition
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