Function of formyl peptide receptor 2 in adriamycin resistance of breast cancer.

IF 2.8 4区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL
Experimental Biology and Medicine Pub Date : 2025-01-15 eCollection Date: 2024-01-01 DOI:10.3389/ebm.2024.10281
Landi Su, Jingjing Li, Li Qin, Yang Feng, Dingwen Xu
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引用次数: 0

Abstract

FPRL2 has been shown to be associated with a variety of tumours but has not been well studied in breast cancer. In this study, We combine molecular biology techniques with bioinformatics to analyze the role of FPRL2 in breast cancer and adriamycin resistance. By utilizing bioinformatics, we mine TCGA and GEO public databases to assess FPRL2 expression in breast cancer patients and its correlation with patient prognosis. Additionally, we employ the DepMap tool to probe the CCLE database, examining the relationship between FPRL2 gene effects and adriamycin sensitivity. Chemosensitivity of Adriamycin in breast cancer cells was tested by CCK-8 method. The apoptosis of breast cancer cells was determined by flow cytometry assay. Expression of p-ERK5 and p-AKT was determined by Western blot assay. Our results indicate that the expression level of FPRL2 in tumor tissues of breast cancer patients is significantly higher than that in normal tissues, and it correlates with poor prognosis in patients. Furthermore, the expression level of FPRL2 in tumor tissues of adriamycin-resistant breast cancer patients is also significantly higher than that in adriamycin-sensitive patients. The IC50 (Inhibitory Concentration 50). Of Adriamycin was significantly lower in FPRL2 silenced cells than those control cells. The apoptosis was markedly increased in FPRL2-silenced cells. p-ERK5 and p-AKT in breast cancer cells was significantly reduced after FPRL2 knocked down. In Conclusion, FPRL2 mediates Adriamycin resistance in breast cancer cells, and knockdown of FPRL2 increased apoptosis and decreased Adriamycin resistance in breast cancer cells.

甲酰基肽受体2在乳腺癌阿霉素耐药中的作用。
FPRL2已被证明与多种肿瘤有关,但尚未在乳腺癌中得到充分研究。在这项研究中,我们将分子生物学技术与生物信息学相结合,分析FPRL2在乳腺癌和阿霉素耐药中的作用。我们利用生物信息学方法,挖掘TCGA和GEO公共数据库,评估乳腺癌患者中FPRL2的表达及其与患者预后的关系。此外,我们使用DepMap工具探查CCLE数据库,检查FPRL2基因效应与阿霉素敏感性之间的关系。CCK-8法检测阿霉素对乳腺癌细胞的化疗敏感性。采用流式细胞术检测乳腺癌细胞的凋亡情况。Western blot法检测p-ERK5、p-AKT的表达。我们的研究结果表明,乳腺癌患者肿瘤组织中FPRL2的表达水平明显高于正常组织,并与患者预后不良相关。此外,FPRL2在阿霉素耐药乳腺癌患者肿瘤组织中的表达水平也明显高于阿霉素敏感患者。IC50 (Inhibitory Concentration 50)。FPRL2沉默细胞中阿霉素的含量明显低于对照细胞。fprl2沉默的细胞凋亡明显增加。FPRL2敲除后,乳腺癌细胞中p-ERK5和p-AKT显著降低。综上所述,FPRL2介导了乳腺癌细胞对阿霉素的耐药,敲低FPRL2增加了乳腺癌细胞凋亡,降低了阿霉素耐药。
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
Experimental Biology and Medicine
Experimental Biology and Medicine 医学-医学:研究与实验
CiteScore
6.00
自引率
0.00%
发文量
157
审稿时长
1 months
期刊介绍: Experimental Biology and Medicine (EBM) is a global, peer-reviewed journal dedicated to the publication of multidisciplinary and interdisciplinary research in the biomedical sciences. EBM provides both research and review articles as well as meeting symposia and brief communications. Articles in EBM represent cutting edge research at the overlapping junctions of the biological, physical and engineering sciences that impact upon the health and welfare of the world''s population. Topics covered in EBM include: Anatomy/Pathology; Biochemistry and Molecular Biology; Bioimaging; Biomedical Engineering; Bionanoscience; Cell and Developmental Biology; Endocrinology and Nutrition; Environmental Health/Biomarkers/Precision Medicine; Genomics, Proteomics, and Bioinformatics; Immunology/Microbiology/Virology; Mechanisms of Aging; Neuroscience; Pharmacology and Toxicology; Physiology; Stem Cell Biology; Structural Biology; Systems Biology and Microphysiological Systems; and Translational Research.
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