ANP32E expression in pancreatic cancer is associated with impaired gemcitabine efficacy and poor patient prognosis

IF 2.3 3区生物学 Q3 BIOCHEMICAL RESEARCH METHODS

Molecular and Cellular Probes Pub Date : 2025-04-28 DOI:10.1016/j.mcp.2025.102030

Xiaohong Liu , Yelin Zhao , Li Zhang , Junting Wang , Liaoxin Luo , Shihui Zhang , Qin Zhu , Yuchen Shi , Chenyu Yuan , Qifeng Xiao , Mengran Xiong , Yuanyuan Duan , Hebing Chen , Hongjuan Yao , Lin Cai , Jianwei Zhang , Guangxi Li , Liang Li

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引用次数: 0

Abstract

Purpose

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive and fatal malignancy, although gemcitabine is administered as a single or combined therapeutic agent. Our previous study demonstrated that ANP32E overexpression promoted PDAC cell proliferation. However, whether it affects treatment outcome and clinical prognosis is still unclear. In the present study, we aimed to determine whether ANP32E is negatively associated with the treatment outcome of gemcitabine.

Methods

We collected clinical characteristics and treatment information from a total of 75 PDAC patients to assess the association of ANP32E expression via immunohistochemical (IHC) staining with overall survival (OS) in patients who were or were not treated with gemcitabine-based chemotherapy, followed by a clinical replication study with transcriptomic data from the TCGA database and functional validation experiments involving the knockdown of ANP32E in the Hup-T3 and SU86.86 human pancreatic cancer cell lines.

Results

We demonstrated the interference effect of ANP32E on gemcitabine efficacy and patient prognosis in PDAC patients by using our own clinical samples or publicly available TCGA datasets. Downregulation of ANP32E significantly sensitized Hup-T3 and SU86.86 cells to gemcitabine, which was consistent with the results of the above association studies.

Conclusion

Our findings suggest that ANP32E might serve as a negative biomarker for poor prognosis and a predictive indicator for poor gemcitabine efficacy. These findings suggest that ANP32E might be a potential therapeutic target to help develop effective drugs to overcome gemcitabine resistance and reduce the risk for relapse or metastasis in patients with PDAC.

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胰腺癌中ANP32E表达与吉西他滨疗效受损和患者预后不良相关

目的：胰腺导管腺癌（PDAC）是一种高度侵袭性和致命性的恶性肿瘤，尽管吉西他滨是单一或联合治疗药物。我们之前的研究表明ANP32E过表达促进了PDAC细胞的增殖。然而，是否影响治疗结果和临床预后尚不清楚。在本研究中，我们旨在确定ANP32E是否与吉西他滨治疗结果负相关。方法收集75例PDAC患者的临床特征和治疗信息，通过免疫组化（IHC）染色评估ANP32E表达与接受或未接受吉西他滨化疗的患者总生存期（OS）的关系。随后，利用TCGA数据库的转录组学数据进行了临床复制研究，并在Hup-T3和SU86.86人胰腺癌细胞系中进行了ANP32E敲低的功能验证实验。结果我们通过自己的临床样本或公开的TCGA数据集证明了ANP32E对吉西他滨疗效和PDAC患者预后的干扰作用。ANP32E的下调使Hup-T3和SU86.86细胞对吉西他滨显着增敏，这与上述关联研究的结果一致。结论ANP32E可能是不良预后的阴性生物标志物，也是吉西他滨疗效差的预测指标。这些发现表明，ANP32E可能是一个潜在的治疗靶点，有助于开发有效的药物来克服吉西他滨耐药，降低PDAC患者复发或转移的风险。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Molecular and Cellular Probes 生物-生化研究方法

CiteScore

6.80

自引率

0.00%

发文量

审稿时长

16 days

期刊介绍： MCP - Advancing biology throughâ€“omics and bioinformatic technologies wants to capture outcomes from the current revolution in molecular technologies and sciences. The journal has broadened its scope and embraces any high quality research papers, reviews and opinions in areas including, but not limited to, molecular biology, cell biology, biochemistry, immunology, physiology, epidemiology, ecology, virology, microbiology, parasitology, genetics, evolutionary biology, genomics (including metagenomics), bioinformatics, proteomics, metabolomics, glycomics, and lipidomics. Submissions with a technology-driven focus on understanding normal biological or disease processes as well as conceptual advances and paradigm shifts are particularly encouraged. The Editors welcome fundamental or applied research areas; pre-submission enquiries about advanced draft manuscripts are welcomed. Top quality research and manuscripts will be fast-tracked.