Background: Pancreatic ductal adenocarcinoma (PDAC) is an insidious, rapidly progressing malignancy of the gastrointestinal tract. Due to its dense fibrous stroma and complex tumor microenvironment, neither of which is sensitive to radiotherapy, pancreatic adenocarcinoma is one of the malignancies with the poorest prognosis. Therefore, detailed elucidation of the inhibitory microenvironment of PDAC is essential for the development of novel therapeutic strategies.

Background: Pancreatic cancer is a highly malignant tumor of the digestive system.Objective: Exosomal circular RNA can be used as a biomarker for the early diagnosis of pancreatic cancer.Methods: The expression of various differentially expressed circRNAs in pancreatic cancer tissues was analyzed by gene chip, exosome expression was verified by electron microscopy and Western blotting, and the expression of exosomal circRNA in pancreatic cancer cells, tissues, and plasma were determined by quantitative reverse transcription‐polymerase chain reaction (qRT‐PCR).Results: Compared with healthy controls, hsa_circ_0006220 and hsa_circ_0001666 were highly expressed in exosomes in the plasma of pancreatic cancer patients. The AUC values were 0.7817 for hsa_circ_0006220, 0.8062 for hsa_circ_0001666, and 0.884 for the combined diagnosis. In addition, clinicopathological features revealed that the expression of hsa_circ_0006220 in plasma exosomes from pancreatic cancer patients was associated with CA19‐9 levels (p = 0.0001) and lymph node metastasis (p = 0.0005). The expression of hsa_circ_0001666 was correlated with both tumor size (p = 0.0157) and CA19‐9 level (p = 0.0001).Conclusions: The high expression of exosomal hsa_circ_0001666 and hsa_circ_0006220 suggests that these can be used as new biomarkers for the diagnosis and treatment of pancreatic cancer.

Naringin (Nar) is one of the natural glycosides extracted from pomelo and other citrus fruits. It has various pharmacological activities, including anti‑inflammatory, antioxidant, anti‑proliferative and anti‑cancer. However, the underlying mechanisms by which Nar regulates apoptosis and autophagy in gastric cancer remain unclear. Thus, the present study aimed to assess the therapeutic effect of Nar and the underlying mechanisms. SNU‑1 cell proliferation was determined using Cell Counting Kit‑8 assay. Cell morphological changes were observed under a phase‑contrast microscope. The changes in the cell cycle were determined using flow cytometry analysis and the changes in cell apoptosis were determined using flow cytometry, Hoechst 33258 and TUNEL staining. The protein levels pertaining to the PI3K/AKT pathway and cell apoptosis and autophagy were monitored using western blot analysis. The results demonstrated that Nar significantly inhibited SNU‑1 cell growth and induced cell cycle arrest in the G0/G1 phase and cell apoptosis. Further mechanistic studies demonstrated that Nar blocked the PI3K/AKT pathway, activated cell autophagy and stimulated the expression of apoptosis‑associated protein cleaved caspase 3 and Bax, but decreased the expression of Bcl‑2. Preincubating SNU‑1 cells with 3‑methyladenine, a cell‑autophagy inhibitor, significantly alleviated the effects of Nar in promoting cell apoptosis and cleaved caspase 3 expression. It was concluded that Nar promoted SNU‑1 cell apoptosis via blocking the PI3K/AKT signaling pathway and activating cell autophagy.