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PTPN9 regulates HER3 phosphorylation during trastuzumab treatment and loss of PTPN9 is a potential biomarker for trastuzumab resistance in HER2 positive breast cancer.

作者信息

Azad Abul, Arshad Maryam, Generali Daniele, Feldinger Katharina, Gijsen Merel, Strina Carla, Cappelletti Mariarosa, Andreis Daniele, Leek Russell, Haider Syed, Kellokumpu-Lehtinen Pirkko-Liisa, Roxanis Ioannis, Harris Adrian Llewellyn, Shaaban Abeer Mahmoud, Joensuu Heikki, Kong Anthony

机构信息

Department of Oncology, The Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK.

Institute of Genomic and Cancer Sciences, Vincent Drive, University of Birmingham, Birmingham, UK.

出版信息

Cancer Commun (Lond). 2025 Jan;45(1):68-73. doi: 10.1002/cac2.12632. Epub 2024 Nov 24.

DOI:10.1002/cac2.12632
PMID:39582148
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11758155/
Abstract
摘要

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1
PTPN9 regulates HER3 phosphorylation during trastuzumab treatment and loss of PTPN9 is a potential biomarker for trastuzumab resistance in HER2 positive breast cancer.在曲妥珠单抗治疗期间，蛋白酪氨酸磷酸酶N9（PTPN9）调节人表皮生长因子受体3（HER3）的磷酸化，PTPN9的缺失是HER2阳性乳腺癌中曲妥珠单抗耐药的潜在生物标志物。
Cancer Commun (Lond). 2025 Jan;45(1):68-73. doi: 10.1002/cac2.12632. Epub 2024 Nov 24.
2
HER2/HER3 heterodimers and p21 expression are capable of predicting adjuvant trastuzumab response in HER2+ breast cancer.HER2/HER3异二聚体和p21表达能够预测HER2阳性乳腺癌患者辅助性曲妥珠单抗治疗的反应。
Breast Cancer Res Treat. 2014 May;145(1):33-44. doi: 10.1007/s10549-014-2925-7. Epub 2014 Apr 6.
3
Phosphorylated HER3 and FITC-labeled trastuzumab immunohistochemistry in patients with HER2-positive breast cancer treated with adjuvant trastuzumab.接受辅助性曲妥珠单抗治疗的HER2阳性乳腺癌患者中磷酸化HER3及异硫氰酸荧光素标记曲妥珠单抗的免疫组织化学研究
Med Mol Morphol. 2019 Jun;52(2):106-113. doi: 10.1007/s00795-018-0208-9. Epub 2018 Oct 13.
4
Targeting of the HER2/HER3 signaling axis overcomes ligand-mediated resistance to trastuzumab in HER2-positive breast cancer.针对 HER2/HER3 信号轴可克服曲妥珠单抗治疗 HER2 阳性乳腺癌的配体介导耐药性。
Cancer Med. 2019 Mar;8(3):1258-1268. doi: 10.1002/cam4.1995. Epub 2019 Jan 31.
5
Posttranscriptional upregulation of HER3 by HER2 mRNA induces trastuzumab resistance in breast cancer.HER2 mRNA 转录后上调诱导乳腺癌对曲妥珠单抗耐药。
Mol Cancer. 2018 Aug 2;17(1):113. doi: 10.1186/s12943-018-0862-5.
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The Hippo Transducer YAP/TAZ as a Biomarker of Therapeutic Response and Prognosis in Trastuzumab-Based Neoadjuvant Therapy Treated HER2-Positive Breast Cancer Patients.在基于曲妥珠单抗的新辅助治疗的HER2阳性乳腺癌患者中，河马转导蛋白YAP/TAZ作为治疗反应和预后的生物标志物
Front Pharmacol. 2020 Aug 27;11:537265. doi: 10.3389/fphar.2020.537265. eCollection 2020.
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HER3, p95HER2, and HER2 protein expression levels define multiple subtypes of HER2-positive metastatic breast cancer.HER3、p95HER2 和 HER2 蛋白表达水平定义了多种 HER2 阳性转移性乳腺癌亚型。
Breast Cancer Res Treat. 2013 Aug;141(1):43-53. doi: 10.1007/s10549-013-2665-0.
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NRG1-dependent activation of HER3 induces primary resistance to trastuzumab in HER2-overexpressing breast cancer cells.NRG1 依赖性激活 HER3 诱导 HER2 过表达乳腺癌细胞对曲妥珠单抗的原发耐药。
Int J Oncol. 2017 Nov;51(5):1553-1562. doi: 10.3892/ijo.2017.4130. Epub 2017 Sep 21.
9
Combination of antibody that inhibits ligand-independent HER3 dimerization and a p110α inhibitor potently blocks PI3K signaling and growth of HER2+ breast cancers.抗体抑制配体非依赖性 HER3 二聚化与 p110α 抑制剂联合，可强力阻断 PI3K 信号通路并抑制 HER2+乳腺癌的生长。
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Dual blockade of HER2 in HER2-overexpressing tumor cells does not completely eliminate HER3 function.在 HER2 过表达的肿瘤细胞中双重阻断 HER2 并不能完全消除 HER3 的功能。
Clin Cancer Res. 2013 Feb 1;19(3):610-9. doi: 10.1158/1078-0432.CCR-12-2024. Epub 2012 Dec 5.

引用本文的文献

1
Comparison of pathological complete response (pCR) between short-term (<6 cycles) and long-term (≥6 cycles) neoadjuvant trastuzumab therapy for HER2-positive breast cancer: a systematic review and meta-analysis of randomized controlled trials.HER2阳性乳腺癌短期（<6周期）与长期（≥6周期）新辅助曲妥珠单抗治疗的病理完全缓解（pCR）比较：一项随机对照试验的系统评价和荟萃分析
Gland Surg. 2025 Jun 30;14(6):1079-1090. doi: 10.21037/gs-2025-25. Epub 2025 Jun 26.

本文引用的文献

1
Neratinib could be effective as monotherapy or in combination with trastuzumab in HER2-low breast cancer cells and organoid models.奈拉替尼可能对 HER2 低表达乳腺癌细胞和类器官模型具有单药或联合曲妥珠单抗的治疗效果。
Br J Cancer. 2024 Jun;130(12):1990-2002. doi: 10.1038/s41416-024-02665-z. Epub 2024 Apr 10.
2
Nuclear HER4 mediates acquired resistance to trastuzumab and is associated with poor outcome in HER2 positive breast cancer.细胞核HER4介导对曲妥珠单抗的获得性耐药，并与HER2阳性乳腺癌的不良预后相关。
Oncotarget. 2014 Aug 15;5(15):5934-49. doi: 10.18632/oncotarget.1904.
3
ADAM10 mediates trastuzumab resistance and is correlated with survival in HER2 positive breast cancer.
ADAM10介导曲妥珠单抗耐药，并与HER2阳性乳腺癌的生存相关。
Oncotarget. 2014 Aug 30;5(16):6633-46. doi: 10.18632/oncotarget.1955.
4
HER2 phosphorylation is maintained by a PKB negative feedback loop in response to anti-HER2 herceptin in breast cancer.HER2 磷酸化通过 PKB 负反馈环维持，以响应乳腺癌中的抗 HER2 赫赛汀。
PLoS Biol. 2010 Dec 21;8(12):e1000563. doi: 10.1371/journal.pbio.1000563.
5
Protein-tyrosine phosphatase PTPN9 negatively regulates ErbB2 and epidermal growth factor receptor signaling in breast cancer cells.蛋白酪氨酸磷酸酶 PTPN9 负调控乳腺癌细胞中的 ErbB2 和表皮生长因子受体信号。
J Biol Chem. 2010 May 14;285(20):14861-14870. doi: 10.1074/jbc.M109.099879. Epub 2010 Mar 24.
6
Protein tyrosine phosphatase PTPN13 negatively regulates Her2/ErbB2 malignant signaling.蛋白酪氨酸磷酸酶PTPN13负向调节Her2/ErbB2恶性信号传导。
Oncogene. 2008 Apr 17;27(18):2525-31. doi: 10.1038/sj.onc.1210922. Epub 2007 Nov 5.
7
Identification of the tyrosine phosphatase PTP-MEG2 as an antagonist of hepatic insulin signaling.酪氨酸磷酸酶PTP-MEG2作为肝脏胰岛素信号拮抗剂的鉴定。
Cell Metab. 2006 May;3(5):367-78. doi: 10.1016/j.cmet.2006.03.006.
8
Adjuvant docetaxel or vinorelbine with or without trastuzumab for breast cancer.辅助多西他赛或长春瑞滨联合或不联合曲妥珠单抗用于乳腺癌治疗。
N Engl J Med. 2006 Feb 23;354(8):809-20. doi: 10.1056/NEJMoa053028.
9
PTEN activation contributes to tumor inhibition by trastuzumab, and loss of PTEN predicts trastuzumab resistance in patients.PTEN激活有助于曲妥珠单抗抑制肿瘤，而PTEN缺失预示着患者对曲妥珠单抗耐药。
Cancer Cell. 2004 Aug;6(2):117-27. doi: 10.1016/j.ccr.2004.06.022.
10
Development of "substrate-trapping" mutants to identify physiological substrates of protein tyrosine phosphatases.开发“底物捕获”突变体以鉴定蛋白酪氨酸磷酸酶的生理底物。
Proc Natl Acad Sci U S A. 1997 Mar 4;94(5):1680-5. doi: 10.1073/pnas.94.5.1680.