PRIM2 通过与 FAM111B 相互作用促进胰腺导管腺癌的增殖和转移。

IF 2.8 4区医学 Q2 ONCOLOGY

Medical Oncology Pub Date : 2024-11-18 DOI:10.1007/s12032-024-02554-8

Jingyang Yin, Fanbo Qin, Hui Chen, Xianxing Wang, Renpei Xia, Bing Ni, Huaizhi Wang

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引用次数: 0

摘要

背景：胰腺导管腺癌（PDAC）是对人类构成巨大威胁的极端恶性肿瘤。PRIM2被报道为肿瘤标志物，但其在PDAC中的功能和调控机制仍不清楚。本研究旨在探讨PRIM2在PDAC中的功能：方法：采用免疫组化（IHC）、Western 印迹和实时定量 PCR（RT-qPCR）方法检测 PRIM2 的表达。细胞实验和异种移植模型证实了这些表型。蛋白质相互作用采用了共免疫沉淀（Co-IP）和蛋白质稳定性测定法：结果：抑制 PRIM2 会导致体外和体内增殖和迁移减少。结果：抑制 PRIM2 会降低体外和体内的增殖和迁移，PRIM2 会上调 FAM111B 的 RNA 水平和蛋白质稳定性：结论：PRIM2/FAM111B轴通过调节PI3K/AKT和上皮-间质转化（EMT）标志物促进增殖和迁移。该轴有望成为治疗 PDAC 的靶点。

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PRIM2 promotes proliferation and metastasis of pancreatic ductal adenocarcinoma through interactions with FAM111B.

Background: Pancreatic ductal adenocarcinomas (PDAC) are huge threat to human for the extreme malignancy. PRIM2 was reported as tumor marker, while the functions and regulatory mechanisms in PDAC are still unclear. The study aimed to investigate the function of PRIM2 in PDAC.

Methods: Expression was detected using immunohistochemistry (IHC), Western blot, and real-time quantitative PCR (RT-qPCR) methods. Cell assays and xenograft model confirmed the phenotypes. Co-Immunoprecipitation (Co-IP) and protein stability assays were used for protein interactions.

Results: Inhibiting PRIM2 resulted in decreased proliferation and migration both in vitro and in vivo. PRIM2 upregulated FAM111B at increased RNA levels and protein stability.

Conclusion: PRIM2/FAM111B axis promoted proliferation and migration by modulating the PI3K/AKT and epithelial-mesenchymal transition (EMT) markers. The axis has the potential to be targeted for PDAC treatment.

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来源期刊

Medical Oncology 医学-肿瘤学

CiteScore

4.20

自引率

2.90%

发文量

259

审稿时长

1.4 months

期刊介绍： Medical Oncology (MO) communicates the results of clinical and experimental research in oncology and hematology, particularly experimental therapeutics within the fields of immunotherapy and chemotherapy. It also provides state-of-the-art reviews on clinical and experimental therapies. Topics covered include immunobiology, pathogenesis, and treatment of malignant tumors.