Objective To summarize the role of exosomal proteins in the occurrence, development, and diagnosis and treatment of pancreatic cancer, providing a reference for the exploration of biomarkers and therapeutic targets in this field. MethodA systematic review of recent domestic and international literature on the mechanisms of exosomes and their proteins in pancreatic cancer was conducted. ResultsProteins carried by tumor-derived exosomes, such as galectin-3 binding protein, V-set andimmunoglobulin domain containing 2, Zrt- and Irt-like protein 4, aspartate aminotransferase 1, could effectively regulate the tumor microenvironment and influence the cell behavior, playing an important role in the occurrence, progression, and metastasis of pancreatic cancer. Additionally, exosomal proteins could serve as potential biomarkers for the early diagnosis of pancreatic cancer. For example, exosomal membrane proteins DNAJ heat shock protein family (HSP40) member B11, and glypican 1 were highly expressed in pancreatic cancer tissues, indicating their potential. ConclusionExosomal proteins are expected to become novel biomarkers and intervention targets for the early diagnosis and targeted therapy of pancreatic cancer, providing new ideas for improving the diagnosis and treatment of pancreatic cancer.
ObjectiveTo summarize the research progress on cell cycle dysregulation in pancreatic ductal adenocarcinoma (PDAC), to explore its roles in PDAC development, malignant biological behavior, and therapeutic resistance, and to provide references for the optimization of cell cycle-related targeted therapeutic strategies. MethodsRelevant studies published in recent years on the role of cell cycle dysregulation in the development of PDAC were systematically retrieved and reviewed. ResultsCell cycle dysregulation is involved in multiple stages of PDAC development and progression, promoting sustained tumor cell proliferation, therapeutic resistance, and malignant progression. Therapeutic strategies targeting key cell cycle regulators, including CDK4/6, ATR, CHK1, and WEE1, have shown promising potential. However, the efficacy of monotherapy remains limited, and further optimization of combination strategies and patient selection is still needed. ConclusionsCell cycle dysregulation is an important biological basis for PDAC development and therapeutic resistance, and it also represents a potential therapeutic entry point. Further clarification of its molecular mechanisms and optimization of biologically guided combination strategies may provide new directions for improving PDAC treatment.