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HER2 RIME experiment from breast cancer specimen

ABSTRACT: RIME targeting ERBB2 (HER2) proteins was performed to analyse ERBB2 interactome to screen novel breast cancer diagnostic markers.

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Atsushi Yokoyama

PROVIDER: PXD061456 | JPOST Repository | Tue Sep 09 00:00:00 BST 2025

REPOSITORIES: jPOST

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			Action	DRS
	349_Sawatsubashi_1_TH_BC83_IgG1_FusionIT.raw	Raw
	351_Sawatsubashi_1_TH_BC86_IgG_1_FusionIT.raw	Raw
	351_Sawatsubashi_2_TH_BC83_IgG2_FusionIT.raw	Raw
	353_Sawatsubashi_2_TH_BC86_IgG_2_FusionIT.raw	Raw
	353_Sawatsubashi_3_TH_BC83_IgG3_FusionIT.raw	Raw

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Publications

HER2 Interactome Profiling Reveals MARCKS as a Candidate Marker Associated with Aggressive Breast Cancer.

Yokoyama Atsushi A Sawatsubashi Shun S Ebata Akiko A Miki Yasuhiro Y Otsubo Yuri Y Suzuki Takashi T

Cancers 20250902 17

<b>Background/Objectives:</b> HER2, a critical diagnostic marker and therapeutic target in breast cancer, is a membrane receptor that forms diverse signaling complexes, the constituents of which have not been fully characterized in actual breast cancer tissues. <b>Methods:</b> In this study, we applied the Rapid Immunoprecipitation Mass Spectrometry of Endogenous Proteins (RIME) method, originally developed to explore transcription factor complexes, to identify the complexes formed by HER2 in HE ...[more]

PMID: 40940979

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HER2 RIME experiment from breast cancer specimen 2

Project description:RIME targeting ERBB2 (HER2) proteins was performed to analyse ERBB2 interactome to screen novel breast cancer diagnostic markers.

2025-09-09 | PXD066103 | JPOST Repository

HER2 RIME experiment from SK-BR-3

Project description:RIME targeting ERBB2 (HER2) proteins was performed to compare ERBB2 immunoprecipitation efficiency and the quality of the interactome.

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RNA-seq of HER2-positive breast cancer BT474 cell line in response to KDM5 ihibition

Project description:Alterations in the histone methylation profiles are observed in various types of cancer and targeting of this epigenetic process has therapeutic potential. Here we provide proof-of-principle that pharmacological targeting of KDM5 histone-demethylases is a new strategy for the personalized treatment of HER2-positive breast cancer. This analysis demonstrates that cells characterized by HER2-positivity are particularly sensitive to KDM5 inhibition. The results are confirmed in an appropriate in vivo model with a close structural analogue (KDM5-inh1A). In selected HER2-positive breast cancer cells, we demonstrate synergistic interactions between KDM5-inh1 and HER2-targeting agents (trastuzumab and lapatinib). In addition, HER2-positive cell lines showing innate/acquired resistance to trastuzumab show sensitivity to KDM5-inh1. The levels of KDM5A/B/C proteins, which are selectively targeted by the agent, have no significant association with KDM5-inh1 responsiveness across our panel of breast cancer cell lines, suggesting the existence of other determinants of sensitivity. Using RNA-sequencing data of the breast cancer cell lines, we generate a gene-expression model, consisting of fifteen genes, which is a robust predictor of KDM5-inh1 sensitivity. In a test set of breast cancers, this model correctly predicts sensitivity to the compound in a large fraction of HER2+ tumors. In conclusion, KDM5 inhibition has potential in the treatment of HER2+ breast cancer and our gene-expression model can be developed into a diagnostic tool to select patients who may benefit from treatments based on KDM5-inhibitors.

2019-02-01 | E-MTAB-7433 | biostudies-arrayexpress

A Myc transcriptional program that is independent of EMT drives a poor prognosis tumor-propagating phenotype in HER2+ breast cancer

Project description:The HER2 (ERBB2) and MYC genes are commonly amplified genes in breast cancer, yet little is known about their molecular and clinical interaction. Using a novel chimeric mammary transgenic approach and in vitro models, we demonstrate markedly increased self renewal and tumour propagating capability of cells transformed with Her2 and c-Myc. Co-expression of both oncogenes in cultured cells led to a pronounced activation of a c-Myc transcriptional signature and acquisition of a self renewing phenotype independent of an EMT programme or regulation of cancer stem cell markers. We show that HER2 and c-MYC are frequently co-amplified in a clinical breast cancer cohort and that co-amplification is strongly associated with aggressive clinical behaviour and poor outcome. Lastly, we show that in patients receiving adjuvant chemotherapy (but not targeted anti-HER2 therapy), MYC amplification is associated with a poor outcome in HER2+ breast cancer patients. These findings demonstrate the importance of molecular context in oncogenic transformation and acquisition of a malignant stem-like phenotype and have important diagnostic and therapeutic consequences for the clinical management of HER2+ breast cancer. Gene expression analysis of Her2, Myc, and Her2 + Myc over expression on MCF10A cells, with MCF10A vector control comparison

2013-09-24 | E-GEOD-43730 | biostudies-arrayexpress

A Myc transcriptional program that is independent of EMT drives a poor prognosis tumor-propagating phenotype in HER2+ breast cancer

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Molecular characterization of Georgia cohort of primary breast cancer FFPE tissues on custom breast cancer DASL panel

Project description:Analysis of 143 formalin-fixed, paraffin-embedded (FFPE) primary breast tumors using a Custom Breast Cancer Panel and Human Cancer Panel for the DASL platform. Molecular markers between the pathology defined subtypes of breast cancer were assessed to hypothesize potential therapeutic targets specific to the subtypes Molecular Characterization of 143 primary breast carcinomas including 101 triple negative (TN: ER-, PR-, HER2-), 3 HER2-positive (HER2+: ER-, PR-, HER2+), and 39 hormone receptor-positive (HR+: ER+ and/or PR+)

2009-10-23 | E-GEOD-18539 | biostudies-arrayexpress

Microarray gene expression profiles from female ER-positive HER2-normal breast cancer patients

Project description:Diagnostic samples from female breast cancer patients with ER-positive and HER2-normal tumors selected for neoadjuvant chemotehrapy.

2023-05-09 | GSE231629 | GEO

Identification of ChIP-seq and RIME grade antibodies for Estrogen Receptor alpha

Project description:Estrogen Receptor alpha (ERα) is a key driver of most breast cancers, and it is the target of endocrine therapies used in the clinic to treat women with ERα positive (ER+) breast cancer. The two methods ChIP-seq (chromatin immunoprecipitation coupled with deep sequencing) and RIME (Rapid Immunoprecipitation of Endogenous Proteins) have greatly improved our understanding of ERα function during breast cancer progression and in response to anti-estrogens. A critical component of both ChIP-seq and RIME protocols is the antibody that is used to pull down the bait protein. To date, most of the ChIP-seq and RIME experiments for the study of ERα have been performed using the sc-543 antibody from Santa Cruz Biotechnology. However, this antibody has been discontinued, thereby severely impacting the study of ERα in normal physiology as well as diseases such as breast cancer and ovarian cancer. Here, we compare the sc-543 antibody with other commercially available antibodies, and we show that 06-935 (EMD Millipore) and ab3575 (Abcam) antibodies can successfully replace the sc-543 antibody for ChIP-seq and RIME experiments.

2019-03-21 | PXD012930 | Pride

Profiling Protein Post-Translational Modifications in Plasma-derived Extracellular Vesicles as Fingerprints for Breast Cancer Subtypes

Project description:Addressing tumor heterogeneity in breast cancer research is crucial, given the distinct subtypes like triple-negative, luminal A/B, and HER2, requiring precise differentiation for effective treatment. This study introduces a non-invasive method by analyzing post-translationally modified proteins in plasma extracellular vesicles (EVs), which play a role in immune regulation and intercellular communication. Examining modifications like phosphorylation, acetylation, and glycosylation in EVs provides insights into breast cancer dynamics. One hundred one plasma samples from luminal A/B, triple-negative breast cancer, and healthy individuals underwent discovery and validation experiments. The study identified over 28,000 unique non-modified peptides, 5,000 phosphopeptides, 680 acetyl peptides, and 1,300 glycopeptides that were successfully characterized. Bioinformatics analyses revealed significant overexpression of 815 non-modified proteins, 3,958 phosphopeptides, 352 acetyl peptides, and 895 glycopeptides in luminal A/B or triple-negative breast cancer subtypes. Phosphorylated and glycosylated PD-L1 peptides emerged as potential markers for breast cancer, regardless of subtype. Aligning findings with literature and PAM50 gene signatures highlighted markers correlated with lower survival rates. The study also conducted 123 scheduled parallel reaction monitoring (PRM) analyses, leveraging machine learning to pinpoint a panel of specific modification sites with high accuracy in subtype differentiation. This research reveals diagnostic markers and enhances understanding of the molecular landscape, contributing to more effective and personalized breast cancer diagnostics and treatments.

2025-11-01 | PXD057412 | JPOST Repository

ER-RIME in wt-MCF7 and MCF7-LTED

Project description:Wild type (wt) MCF7 cells, modelling breast cancer at primary diagnosis, were cultured in phenol red-free RPMI supplemented with 10% FBS and 1nM estradiol (E2). Long-term oestrogen deprived (LTED) cell lines, which model resistance to endocrine therapy, were cultured in phenol red-free RPMI in the absence of exogenous E2 and supplemented with 10% dextran charcoal-stripped bovine serum (DCC). Samples were harvested at baseline and at the point of resistance (LTED). In order to do comparative analysis in the ER-interactome of wt-MCF7 and MCF7-LTED cells, ER-RIME (rapid immunoprecipitation mass spectrometry of endogenous proteins) was conducted in these cells.

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