Song Lanying, Cai Renming
Department of Endocrinology and Metabolic Diseases, Suining Hospital of Traditional Chinese Medicine Affiliated to North Sichuan Medical College Suining 629000, Sichuan, China.
Department of Pharmacy, Lezhi County People's Hospital Ziyang 641500, Sichuan, China.
Am J Transl Res. 2025 Aug 15;17(8):5885-5895. doi: 10.62347/TTQJ2494. eCollection 2025.
To explore the effects of baicalein on immune cell infiltration and tumor progression in pancreatic cancer by modulating DDX60 expression.
RNA-seq data of pancreatic cancer and normal tissues were obtained from the UCSC XENA database. DDX60 expression differences and their associations with patient prognosis and immune infiltration were analyzed. Panc02 pancreatic cancer cells were treated with baicalein (0, 20, 40, 60 μmol/L) for 24, 48, and 72 hours. Cell viability was assessed by MTT assay, while apoptosis and DDX60 expression were evaluated by flow cytometry and RT-qPCR, respectively. In vivo, tumor-bearing mice received baicalein, and tumor volume, immune cell infiltration, and DDX60 expression in tumor tissues were assessed.
DDX60 expression was significantly upregulated in pancreatic cancer tissues compared to normal tissues (P < 0.05). Patients with low DDX60 had better survival (P < 0.05). DDX60 levels correlated significantly with multiple immune cell types, including DCs, eosinophils, macrophages, neutrophils, T cell subsets, and NK cells (P < 0.05). Baicalein inhibited Panc02 cell proliferation and induced apoptosis in a dose- and time-dependent manner (P < 0.05), accompanied by downregulation of DDX60 (P < 0.05). In vivo, baicalein significantly suppressed tumor growth and increased CD8 T cells and macrophages in tumor tissues (P < 0.05). DDX60 expression decreased with increasing baicalein dosage (P < 0.05).
Baicalein suppresses pancreatic cancer growth and promotes apoptosis, apparently through downregulation of DDX60 and modulation of immune responses in the tumor microenvironment.
通过调节DDX60表达，探讨黄芩苷对胰腺癌免疫细胞浸润和肿瘤进展的影响。
从UCSC XENA数据库获取胰腺癌和正常组织的RNA测序数据。分析DDX60表达差异及其与患者预后和免疫浸润的关联。用黄芩苷（0、20、40、60μmol/L）处理Panc02胰腺癌细胞24、48和72小时。通过MTT法评估细胞活力，同时分别通过流式细胞术和RT-qPCR评估细胞凋亡和DDX60表达。在体内，给荷瘤小鼠注射黄芩苷，评估肿瘤体积、肿瘤组织中的免疫细胞浸润和DDX60表达。
与正常组织相比，胰腺癌组织中DDX60表达显著上调（P<0.05）。DDX60低表达的患者生存期较好（P<0.05）。DDX60水平与多种免疫细胞类型显著相关，包括树突状细胞、嗜酸性粒细胞、巨噬细胞、中性粒细胞、T细胞亚群和自然杀伤细胞（P<0.05）。黄芩苷以剂量和时间依赖性方式抑制Panc02细胞增殖并诱导凋亡（P<0.05），同时伴随DDX60下调（P<0.05）。在体内，黄芩苷显著抑制肿瘤生长，并增加肿瘤组织中的CD8 T细胞和巨噬细胞（P<0.05）。DDX60表达随黄芩苷剂量增加而降低（P<0.05）。
黄芩苷通过下调DDX60和调节肿瘤微环境中的免疫反应，明显抑制胰腺癌生长并促进凋亡。
