Background: Pancreatic cancer, while relatively uncommon, is extrapolated to become the second leading cause of cancer-related deaths worldwide. Despite identifying well-known markers like theKRASgene, the exact regulation of pancreatic cancer progression remains elusive.Methods: Clinical value of PRC1 was analyzed using bioinformatics database. The role of PRC1 was further evaluated through cell-based assays, including viability, wound healing, and sensitivity with the drug.Results: We demonstrate that PRC1 was significantly overexpressed in pancreatic cancer compared to pancreases without cancer, as revealed through human databases and cell lines analysis. Furthermore, high PRC1 expression had a negative correlation with CD4+ T cells, which are crucial for the immune response against cancers. Additionally, PRC1 showed a positive correlation with established pancreatic cancer markers. Silencing PRC1 expression using siRNA significantly inhibited cancer cell proliferation and viability and increased chemotherapeutic drug sensitivity.Conclusions: These findings suggest that targeting PRC1 in pancreatic cancer may enhance immune cell infiltration and inhibit cancer cell proliferation, offering a promising avenue for developing anticancer therapies.
背景：胰腺癌虽相对少见，但预计将成为全球癌症相关死亡的第二大原因。尽管已发现如KRAS基因等已知标志物，但胰腺癌进展的确切调控机制仍不明确。 方法：通过生物信息学数据库分析PRC1的临床价值，并进一步通过细胞实验（包括细胞活力、伤口愈合及药物敏感性检测）评估PRC1的作用。 结果：人类数据库及细胞系分析显示，与正常胰腺组织相比，PRC1在胰腺癌中显著过表达。此外，PRC1高表达与对癌症免疫应答至关重要的CD4+ T细胞呈负相关，同时与已确认的胰腺癌标志物呈正相关。使用siRNA沉默PRC1表达可显著抑制癌细胞增殖与活力，并增强化疗药物敏感性。 结论：这些发现表明，靶向PRC1可能增强胰腺癌中的免疫细胞浸润并抑制癌细胞增殖，为开发抗癌疗法提供了新方向。
Modulation of PRC1 Promotes Anticancer Effects in Pancreatic Cancer
肿瘤(癌症)患者之家