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Site-specific glycan analysis of ErbB2 in breast cancer cell SKBR-3

ABSTRACT: This study provides site-specific profiles of asparagine-linked and serine/threonine-linked glycosylations on ErbB2, a therapeutic target RTK for ErbB2-positive cancer, through structural analysis of recombinant ErbB2 extracellular region and endogenous ErbB2 from ErbB2-positive breast cancer cells.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell

DISEASE(S): Breast Cancer

SUBMITTER: Naoki Fujitani

LAB HEAD: Motoko Takahashi

PROVIDER: PXD039837 | Pride | 2024-05-24

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ErbB2.fasta	Fasta
	SKBR3_IP.raw	Raw
	allPeptides.txt	Txt
	allSpectra.HCD.FTMS.iso_0.apl	Other
	allSpectra.HCD.FTMS.iso_1.apl	Other

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1 - 5 of 32

Publications

Site-specific glycosylation analysis of epidermal growth factor receptor 2 (ErbB2): exploring structure and function toward therapeutic targeting.

Fujitani Naoki N Uehara Yasuaki Y Ariki Shigeru S Hashimoto Ukichiro U Mukai Jo J Hasegawa Yoshihiro Y Takahashi Motoko M

Glycobiology 20240401 3

Glycans found on receptor tyrosine kinases (RTKs) have emerged as promising targets for cancer chemotherapy, aiming to address issues such as drug resistance. However, to effectively select the target glycans, it is crucial to define the structure and function of candidate glycans in advance. Through mass spectrometric analysis, this study presents a "glycoform atlas" of epidermal growth factor receptor 2 (ErbB2), an RTK targeted for the treatment of ErbB2-positive cancers. Our analysis provides ...[more]

PMID: 38109791

Similar Datasets

Site-specific glycan analysis of epidermal growth factor receptor 2

Project description:This study provides site-specific profiles of asparagine-linked and serine/threonine-linked glycosylations on ErbB2, a therapeutic target RTK for ErbB2-positive cancer, through structural analysis of recombinant ErbB2 extracellular region and endogenous ErbB2 from ErbB2-positive breast cancer cells. Furthermore, comparison of the N-glycosylated structures of the extracellular regions of ErbB2 and its homologue, the epidermal growth factor receptor (EGFR), showed differences in the distribution and density of N-glycans on both molecules, providing new insights into the different activation mechanisms of ErbB2 and EGFR from a glycan perspective.

2024-05-21 | PXD039834 | Pride

Site-specific glycan analysis of CHO cell expressed epidermal growth factor receptor 2

2024-05-21 | PXD039835 | Pride

Site-specific glycan analysis of epidermal growth factor receptor (EGFR)

2024-05-24 | PXD039836 | Pride

Site-specific glycan analysis of ErbB2 in breast cancer cell BT474

2024-05-24 | PXD039838 | Pride

ErbB2 Site-Specific α2,6-Sialylation Regulates Gastric Cancer Cell Sensitivity to Trastuzumab

Project description:The clinical performance of trastuzumab in the treatment of ErbB2-positive gastric cancer is severely hampered by the emergence of molecular resistance. The glycosylation landscape of ErbB2’s extracellular domain, and the molecular mechanisms through which it tunes gastric cell malignancy, including the acquisition of trastuzumab resistance, remain elusive. We show that the expression of ErbB2 sialylated glycoforms holds clinical utility in the prediction of clinical outcome and stratification of gastric cancer patients. In-depth glycoproteomic and glycomic analysis of ErbB2 extracellular region disclosed a site-specific profile in gastric cancer cells. We further demonstrate that ST6Gal1 sialyltransferase specifically targets ErbB2 N-glycosylation sites within the trastuzumab binding domain. Moreover, the abrogation of ST6Gal1-mediated α2,6-sialylation reshapes ErbB2 glycome and sensitizes gastric cancer cells to trastuzumab-induced cytotoxicity through receptor membrane stabilization and a downregulation of ErbB2 activation. Overall, this data demonstrates that aberrant sialylation tunes the molecular resistance of ErbB2-driven gastric cancer cells to trastuzumab.

2021-05-11 | PXD017609 | Pride

Redifferentiated cardiomyocytes retain residual dedifferentiation signatures and are protected against ischaemic injury

Project description:Near-complete reversal of ERBB2-driven cardiomyocyte dedifferentiation is driven by the Hippo pathway, restoring contractility whilst long-lasting conferring cardioprotection.

2023-02-01 | PXD038450 | Pride

Transcription profiling of cancer progression to study the intrinsic regulation of transforming growth factor-beta signaling in ErbB2/Neu-induced tumors

Project description:To identify early events of erbB2-induced mammary tumorigenesis, we compared datasets from 14 genechip experiments including MMTV-neu tumors, preneoplastic neu mammary gland (adjacent neu), and age-matched, wild-type control mammary glands

2007-09-04 | E-GEOD-2528 | biostudies-arrayexpress

Activation of different signaling pathways in the regulation of biological properties of human pancreatic cancer cells by the mucin MUC4 and the oncogenic receptor ErbB2 genes

Project description:The mucin MUC4 and its membrane partner the ErbB2 oncogenic receptor are potential actors and partners in pancreatic tumourigenesis. However, the way they function is still largely unknown. We thus undertook in this work to identify the cellular mechanisms and the intracellular signalling pathways under the control of both ErbB2 and MUC4. Using co-immunoprecipitation, we show that MUC4 and ErbB2 interact in the human pancreatic adenocarcinomatous cell line CAPAN-2. Stable Knocked-Down (KD) cellular clones for both MUC4 and ErbB2 were raised by a shRNA approach. Biological properties of these cells were then studied in vitro and in vivo. Our results show that ErbB2-KD cells are more apoptotic and less proliferative (decreased cyclin D1 and increased p27kip1 expression) while migration and invasive properties were not altered. MUC4-KD clones were less proliferative with decreased cyclin D1 expression, G1 cell cycle arrest and altered ErbB2/ErbB3 expression. Their migration properties were reduced whereas invasive properties were increased. Importantly, inhibition of ErbB2 and MUC4 expression did not impair the same signalling pathways (inhibition of MUC4 expression affected the JNK pathway whereas that of ErbB2 altered the MAPK pathway). Finally, ErbB2-KD and MUC4-KD cells showed impaired tumour growth in vivo. This indicates that ErbB2 and MUC4, that physically interact, activate different intracellular signalling pathways to regulate biological properties of pancreatic cancer cells. Altogether, these data bring new information regarding molecular mechanisms under the control of both MUC4 and ErbB2 that will have to be taken into account for developing efficient targeting of both proteins in order to slow down/stop pancreatic tumourigenesis. profiling of pancreatic cells depleted for ErbB2 and MUC4

2012-03-20 | E-GEOD-31322 | biostudies-arrayexpress

Identification of p130Cas/ErbB2-dependent invasive signatures in transformed mammary epithelial cells

Project description:Understanding transcriptional changes during cancer progression is of crucial importance to develop new and more efficacious diagnostic and therapeutic approaches. It is well known that ErbB2 is overexpressed in about 25% of human invasive breast cancers. We have previously demonstrated that p130Cas overexpression synergizes with ErbB2 in mammary cell transformation and promotes ErbB2-dependent invasion in three-dimensional (3D) cultures of human mammary epithelial cells. Here, by comparing coding and non-coding gene expression profiles, we define the invasive signatures associated with concomitant p130Cas overexpression and ErbB2 activation in 3D cultures of mammary epithelial cells. Specifically, we have found that genes involved in amino acids synthesis (CBS, PHGDH), cell motility, migration (ITPKA, PRDM1), and angiogenesis (HEY1) are upregulated, while genes involved in inflammatory response (SAA1, S100A7) are downregulated. In parallel, we have shown that the expression of specific miRNAs is altered. Among these, miR-200b, miR-222, miR-221, miR-R210, and miR-424 are upregulated, while miR-27a, miR-27b, and miR-23b are downregulated. Overall, this study presents, for the first time, the gene expression changes underlying the invasive behavior following p130Cas overexpression in an ErbB2 transformed mammary cell model. To identify transcriptional changes occurring during invasion we have performed a comparative microarray analysis of non coding RNA (miRNA) between MCF10A.B2 acini over-expressing p130Cas with activation of ErbB2 and control cells.

2013-07-22 | E-GEOD-42949 | biostudies-arrayexpress

Transcriptomic analysis of mammary tumors from MMTV-ErbB2 transgenic mice

Project description:The tyrosine kinase ErbB2 positive breast tumors have more aggressive tumor growth, poorer clinical outcome, and more resistance to radiotherapy, chemotherapy and hormone therapy. A humanized anti-ErbB2 monoclonal antibody Herceptin and a small molecules inhibitor Lapatinib were developed and approved by FDA to treat patients with ErbB2 amplification and overexpression. Unfortunately, most ErbB2+ breast cancers do not respond to Herceptin and Lapatinib, and the majority of responders become resistant within 12 months of initial therapy (defined as secondary drug resistance). Such differences in response to Lapatinib treatment is contributed by substantial heterogeneity within ErbB2+ breast cancers. To address this possibility, we carried out transcriptomic analysis of mammary tumors from genetically diverse MMTV-ErbB2 mice. This will help us to have a better understanding of the heterogeneous response to ErbB2 targeted therapy and permit us to design better and more individualized (personalized) treatment strategies for human ErbB2 positive breast cancer. 214 MMTV-ErbB2 mammary tumors and 8 normal mammary glands were analyzed by Affymetrix microarrays.

2014-02-01 | E-GEOD-54582 | biostudies-arrayexpress

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