PTBP3 is an RNA-binding protein that regulates pre-mRNA alternative splicing and controls cell proliferation, differentiation, and migration. The protein binds preferentially to poly(G) and poly(U) sequences and mediates exon skipping of multiple target transcripts. PTBP3 is significantly overexpressed across diverse human cancers, including gallbladder, gastric, colorectal, hepatocellular, and lung adenocarcinoma, where elevated expression typically correlates with poor prognosis 1. In gallbladder cancer, PTBP3 promotes IL-18 exon skipping to generate a tumor-specific isoform that facilitates immune escape by suppressing CD8+ T cell activation 2. In gastric cancer peritoneal metastasis, PTBP3 mediates COX11 exon skipping, impairing mitochondrial copper handling and enabling tumor cells to evade cuproptosis 3. In colorectal cancer, PTBP3 stabilizes UBE4A mRNA, leading to P53 degradation and enhanced proliferation 4. Under hypoxic conditions in pancreatic cancer, PTBP3 upregulates ATG12 to promote autophagy-mediated chemoresistance to gemcitabine 5. In lung adenocarcinoma, TGF-β induces PTBP3 expression through Smad3 recruitment, enabling epithelial-to-mesenchymal transition and metastasis 6. Antisense oligonucleotides targeting PTBP3-mediated splicing events have shown anti-tumor activity in preclinical models, suggesting potential therapeutic strategies targeting this splicing factor.