胰腺癌（PC）是癌症相关死亡的主要原因。由于缺乏可靠的生物标志物来预测预后或指导治疗，迫切需要对PC进行分子研究。淋巴细胞抗原 6 家族成员 E (LY6E) 与各种癌症中不受控制的细胞生长有关。然而，LY6E在PC中的确切机制仍不清楚。在这里，我们使用在线工具和 R- × 64-4.1.1 进行了全面的生物信息分析，并通过蛋白质印迹、免疫组织化学、免疫吸附测定、流式细胞术、细胞测定和动物模型进行实验验证。我们的研究结果表明，PC 中 LY6E 的表达显着升高，与不良预后相关。 LY6E 敲低抑制 PC 细胞的增殖、侵袭和迁移，同时增强细胞凋亡，这通过增加裂解的 caspase 3 水平和改变 Bcl-2/Bax 比率来证明。相反，LY6E过表达促进PC细胞增殖和迁移，并抑制细胞凋亡。从机制上讲，LY6E 下调抑制了 Wnt/β-catenin 信号通路。体内研究表明，LY6E 抑制可减弱小鼠模型中的肿瘤生长。此外，LY6E 抑制导致小鼠肿瘤生长减少。总之，我们的研究证实了 LY6E 在 PC 进展中的重要作用。 LY6E 作为独立的预后指标，有潜力成为 PC 的有价值的生物标志物，为治疗策略提供信息。© 2024。作者。

Pancreatic cancer (PC) is the primary cause of cancer-related mortality. Due to the absence of reliable biomarkers for predicting prognosis or guiding treatment, there is an urgent need for molecular studies on PC. Lymphocyte antigen 6 family member E (LY6E) is implicated in uncontrolled cell growth across various cancers. However, the precise mechanism of LY6E in PC remains unclear. Here, we conducted comprehensive bioinformatic analyses using online tools and R- × 64-4.1.1, complemented by experimental validation through Western blotting, immunohistochemistry, immunosorbent assays, flow cytometry, cell assays, and animal models. Our findings reveal significantly elevated expression of LY6E in PC, correlating with poor prognosis. LY6E knockdown inhibited proliferation, invasion, and migration of PC cells, while enhancing apoptosis evidenced by increased cleaved caspase 3 levels and alterations in the Bcl-2/Bax ratio. Conversely, LY6E overexpression promoted PC cell proliferation and migration, and inhibited apoptosis. Mechanistically, LY6E downregulation suppressed the Wnt/β-catenin signaling pathway. In vivo studies demonstrated that LY6E suppression attenuated tumor growth in murine models. Additionally, LY6E suppression resulted in reduced tumor growth in mice. In conclusion, our study confirms the significant role of LY6E in the progression of PC. LY6E, serving as an independent prognostic indicator, has the potential to serve as a valuable biomarker for PC to inform treatment strategies.© 2024. The Author(s).