PRIM2 通过与 FAM111B 相互作用促进胰腺导管腺癌的增殖和转移。
PRIM2 promotes proliferation and metastasis of pancreatic ductal adenocarcinoma through interactions with FAM111B.
机构信息
University of Chinese Academy of Sciences (UCAS) Chongqing School, Chongqing Medical University, Chongqing, P. R. China.
Chongqing Institute of Green and Intelligent Technology, Chinese Academy of Sciences, Chongqing, 400174, P. R. China.
出版信息
Med Oncol. 2024 Nov 18;42(1):6. doi: 10.1007/s12032-024-02554-8.
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.
背景
胰腺导管腺癌（PDAC）因其极高的恶性程度，对人类健康构成了巨大威胁。PRIM2 被报道为肿瘤标志物，但在 PDAC 中的功能和调节机制尚不清楚。本研究旨在探讨 PRIM2 在 PDAC 中的功能。
方法
采用免疫组织化学（IHC）、Western blot 和实时定量 PCR（RT-qPCR）方法检测表达。细胞实验和异种移植模型验证了表型。免疫共沉淀（Co-IP）和蛋白质稳定性实验用于研究蛋白质相互作用。
结果
抑制 PRIM2 可降低体外和体内的增殖和迁移。PRIM2 通过增加 FAM111B 的 RNA 水平和蛋白质稳定性而上调 FAM111B。
结论
PRIM2/FAM111B 轴通过调节 PI3K/AKT 和上皮-间充质转化（EMT）标志物促进增殖和迁移。该轴有可能成为 PDAC 治疗的靶点。
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