Pancreatic cancer is difficult to manage owing to the challenges involved in its treatment and nursing. This study aimed to clarify the roles and mechanisms of action of Poly (A)-binding protein cytoplasmic 1 (PABPC1) on pancreatic cancer. The expression of PABPC1 in pancreatic cancer tissues and cell lines was detected using RT-qPCR and western blotting. The effects of PABPC1 on proliferation, apoptosis, epithelial-mesenchymal transition (EMT), and the PI3K/AKT signaling pathway in pancreatic cancer cells were further investigated using MTT assays, flow cytometry, and western blotting. The expression of PABPC1 was significantly upregulated in pancreatic cancer tissues and cells, whereas PABPC1 downregulation inhibited pancreatic cancer cell proliferation, induced apoptosis, decreased the expression of EMT-associated proteins, and exerted a regulatory effect by inhibiting the PI3K/AKT signaling pathway. In addition, the findings indicated that PABPC1 over-expression significantly promoted pancreatic cancer cell proliferation, inhibited apoptosis, decreased the expression of E-cadherin, enhanced N-cadherin expression, and activating the PI3K/AKT signaling pathway. PABPC1 silencing significantly inhibited proliferation and EMT and induced apoptosis in pancreatic cancer cells. These findings provide novel insights into the role of PABPC1 in the development of pancreatic cancer.

由于治疗和护理方面的挑战，胰腺癌很难治疗。本研究旨在阐明多聚A结合蛋白胞质1（PABPC1）在胰腺癌中的作用和作用机制。采用RT-qPCR和蛋白质印迹法检测胰腺癌组织和细胞系中PABPC1的表达。使用 MTT 测定、流式细胞术和蛋白质印迹进一步研究 PABPC1 对胰腺癌细胞增殖、凋亡、上皮间质转化 (EMT) 和 PI3K/AKT 信号通路的影响。 PABPC1在胰腺癌组织和细胞中表达显着上调，而PABPC1下调则抑制胰腺癌细胞增殖、诱导细胞凋亡、降低EMT相关蛋白表达，并通过抑制PI3K/AKT信号通路发挥调节作用。此外，研究结果表明，PABPC1过表达显着促进胰腺癌细胞增殖、抑制细胞凋亡、降低E-cadherin表达、增强N-cadherin表达、激活PI3K/AKT信号通路。 PABPC1 沉默显着抑制胰腺癌细胞的增殖和 EMT，并诱导细胞凋亡。这些发现为 PABPC1 在胰腺癌发展中的作用提供了新的见解。