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ERBB2 signalling and functions in oesophageal cancer

ABSTRACT: Oesophageal adenocarcinoma (OAC) is a deadly disease with poor survival statistics and few targeted therapies available. One of the most common molecular aberrations in OAC is amplification or activation of the receptor tyrosine kinase ERBB2, and ERBB2 is targeted in the clinic for this subset of patients. However, the downstream consequences of these activating events ERBB2 activation or amplification are not well understood. Here we used a combination of phosphoproteomics, open chromatin profiling and transcriptome analysis on cell line models and patient-derived datasets to interrogate the molecular pathways operating downstream from ERBB2. Integrated analysis of these data sets converge on a model where ERBB2 activity is mediated at the transcriptional level by the transcription factor AP1. AP1 in turn controls cell behaviour by acting on cohorts of genes that regulate cell migration and adhesion, features often associated with EMT. Our study therefore provides a valuable resource for the cancer cell signalling community and reveals novel molecular determinants underlying the dysregulated behaviour of OAC cells.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Gastroesophageal Cancer

SUBMITTER: Chiara Francavilla

LAB HEAD: chiara francavilla

PROVIDER: PXD029180 | Pride | 2023-01-03

REPOSITORIES: Pride

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			Action	DRS
	20191018_CF_collab_SO_SILAC_OE19_STY_01_01.raw	Raw
	20191018_CF_collab_SO_SILAC_OE19_STY_01_01_20191021220355.raw	Raw
	20191018_CF_collab_SO_SILAC_OE19_STY_01_02.raw	Raw
	20191018_CF_collab_SO_SILAC_OE19_STY_01_02_20191021234141.raw	Raw
	20191018_CF_collab_SO_SILAC_OE19_STY_02_01.raw	Raw

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