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RBM10 inhibits pancreatic cancer development by suppressing immune escape through PD-1 expression

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机构： [1]Department of Pathology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. [2]Research Institute of Pancreatic Diseases, Shanghai Key Laboratory of Translational Research for Pancreatic Neoplasms, Shanghai Jiaotong University School of Medicine, Shanghai 200025, China. [3]Department of Pathology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China. [4]Department of Pathology, The Affiliated Taizhou Peoples Hospital of Nanjing Medical University, Taizhou 225300, Jiangsu, China. [5]Department of Pathology, Taizhou School of Clinical Medicine, Nanjing Medical University, Taizhou 225300, Jiangsu, China.

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关键词： PAAD RBM10 JAK-STAT PD-1 NK cell

摘要：

RNA-binding motif protein-10 (RBM10) plays a role in pancreatic adenocarcinoma (PAAD), though its precise underlying mechanism remains unclear. The current study investigates the role of RBM10 in pancreatic cancer progression and immune regulation. RBM10 expression in pancreatic tissues from PAAD patient was assessed using Western blotting, RT-qPCR, and immunohistochemistry, revealing lower levels in pancreatic cancerous tissues compared to adjacent non-cancerous tissues. This finding aligns with in vitro experiments where RBM10 knockdown in pancreatic cancer cells enhanced colony formation, migration, and proliferation, which correlated with increased P-JAK1, P‑JAK2, and P-STAT3 levels. Bioinformatics identified RBM10-related pathways and immune changes. Moreover, RBM10 deficiency in cancer cells increased PD-1 expression in natural killer cells in vitro, reducing their tumour-killing ability. However, treatment with the JAK pathway inhibitor AZD1480 restored NK cell cytotoxicity against cancer cells. Finally, high RBM10 expression was associated with a favourable prognosis in pancreatic cancer patients, suggesting that RBM10 inhibits pancreatic cancer progression by suppressing tumour immune escape through JAK-STAT-mediated regulation of PD-1 expression in NK cells. This finding offers potential for the development of novel precision-targeted therapies in the management of pancreatic cancer.© The author(s).

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出版当年[2025]版：

大类 | 3 区医学

小类 | 4 区肿瘤学

最新[2025]版：

大类 | 3 区医学

小类 | 4 区肿瘤学

第一作者：

第一作者机构： [1]Department of Pathology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. [2]Research Institute of Pancreatic Diseases, Shanghai Key Laboratory of Translational Research for Pancreatic Neoplasms, Shanghai Jiaotong University School of Medicine, Shanghai 200025, China.

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通讯作者：

通讯机构： [1]Department of Pathology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. [2]Research Institute of Pancreatic Diseases, Shanghai Key Laboratory of Translational Research for Pancreatic Neoplasms, Shanghai Jiaotong University School of Medicine, Shanghai 200025, China. [3]Department of Pathology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China. [4]Department of Pathology, The Affiliated Taizhou Peoples Hospital of Nanjing Medical University, Taizhou 225300, Jiangsu, China. [5]Department of Pathology, Taizhou School of Clinical Medicine, Nanjing Medical University, Taizhou 225300, Jiangsu, China.

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