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Effects of EGF, cetuximab, trastuzumab and afatinib on gene expression in gastric cancer cell lines

ABSTRACT: Effects of EGF, cetuximab, trastuzumab and afatinib on gene expression in gastric cancer cell lines

PROVIDER: PRJNA593206 | ENA |

REPOSITORIES: ENA

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Effects of EGF, cetuximab, trastuzumab and afatinib on gene expression in gastric cancer cell lines

Project description:The antibody trastuzumab in combination with platin-fluoropyrimidine chemotherapy is the standard of care for patients with HER2-positive recurrent or metastatic gastric cancer. Alternative treatment options and biomarkers for prediction of therapy response are needed since some patients do not respond to trastuzumab therapy or develop acquired resistance. We compared the molecular effects of trastuzumab and other HER-targeting drugs cetuximab and afatinib. We also tested the hypothesis that the treatment-dependent regulation of a gene indicates its importance for response, and therefore it may be used as biomarker for patient stratification. The four gastric cancer cell lines Hs746T, MKN1, MKN7 and NCI-N87 were treated with EGF, cetuximab, trastuzumab or afatinib for 4 or 24 hours. The effect on gene expression was then measured by RNA sequencing and the resulting candidate biomarkers were tested in an available cohort of gastric cancer patients or were functionally analyzed in vitro. Treatment with afatinib resulted in the highest number of regulated genes, followed by cetuximab and trastuzumab. Although trastuzumab had little effects on gene expression, we identified BMF, HAS2 and SHB as candidate biomarkers for trastuzumab response. HAS2 and SHB were confirmed as potential predictive markers for trastuzumab therapy response in clinical specimens. AREG, EREG and HBEGF were identified as candidate biomarkers for afatinib and cetuximab treatment. The functional analysis confirmed HBEGF as resistance factor for cetuximab. By confirming HAS2, SHB and HBEGF as biomarkers for anti-HER therapies, we provide evidence that the regulation of gene expression after treatment can be used for biomarker discovery.

2020-11-02 | GSE141352 | GEO

Human colon cancer cell lines: NT(untreated) vs EGF, Cetuximab and Gefitinib treatments

Project description:Gene Expression Profiling of HT-29 and Caco-2 colon cancer cell lines untreated compared with EGF, Cetuximab, Gefitinib,EGF plus Cetuximab and EGF plus gefitinib treatments. Keywords: Gene Expression Profiling

2007-09-12 | GSE8967 | GEO

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

Regulation of HB-EGF by miR-212 and acquired cetuximab-resistance in head and neck cancer

2011-01-14 | GSE21483 | GEO

Molecular Atlas of HER2+ Breast Cancer Cells Stimulated with EGF and HRG: Temporal Insights into Mechanisms in Trastuzumab Resistance [RNA-Seq]

Project description:Trastuzumab therapy in HER2+ breast cancer patients have mixed success owing to acquired resistance to therapy. In this study, we investigate the cellular mechanisms underlying acquired resistance using -sensitive and -resistant cancer cells (BT474 and BT474R) treated with endogenous ligands EGF and HRG, across time. Our measurements probe early receptor organization through microscopy, signaling events through multi-omic measurements and assess the cellular energetic state through mitochondrial measurements. Our integrative analyses of these multimodal measurements highlight differential mechanisms in both cell lines in response to ligands. In BT474, an active PI3K-AKT-mTORC1 signaling contributes to an active mitochondrial bioenergetic state (glycolysis and lipid metabolism) for both ligands EGF and HRG. A HIF1A mediated increase in cellular bioenergetics is also seen. In BT474R, there is a ligand-dependent activation of signaling cascades. In EGF treated BT474R, an EGFR driven IRF1/STAT1/STAT2 activation with likely impact on cellular bioenergetics is seen, whilst an AR mediated alteration of lipid metabolism is pronounced after HRG treatment.

2024-02-14 | GSE237606 | GEO

Molecular Atlas of HER2+ Breast Cancer Cells Stimulated with EGF and HRG: Temporal Insights into Mechanisms in Trastuzumab Resistance [ATAC-Seq]

2024-02-14 | GSE237605 | GEO

Regulation of HB-EGF by miR-212 and acquired cetuximab-resistance in head and neck cancer

Project description:To determine the mechanism of cetuximab-resistance in head and neck cancer, a cetuximab-sensitive cell line (SCC1) and its cetuximab-resistant derivative (1Cc8) were analyzed for differentially expressed genes using DNA microarrays. 900 differentially expressed genes were found using the statistical cut-off point of one-way ANOVA with FDR less than 1%. The SCC1 and 1Cc8 cell lines were grown in biological triplicates. Total RNA was isolated and array experiments were performed. The supplementary file 'GSE21483_differentially_expressed_genes.txt' includes the list of differentially expressed genes that were identified.

2011-01-14 | E-GEOD-21483 | biostudies-arrayexpress

Determining the effects of trastuzumab, cetuximab and afatinib by phosphoprotein, gene expression and phenotypic analysis in gastric cancer cell lines.

Project description: Not available

| S-EPMC7594334 | biostudies-literature

RNA sequencing of BT474 cells treated with trastuzumab or trastuzumab + pertuzumab and BT474-derived cells resistant to trastuzumab or trastuzumab + pertuzumab

Project description:We sequenced untreated BT474 cells, BT474 cells treated for three days with trastuzumab or trastuzumab + pertuzumab, as well as two BT474-derived trastuzumab-resistant pools and two BT474-derived trastuzumab + pertuzumab resistant pools. Resistant pools were generated by culturing BT474 cells in gradually increasing doses of trastuzumab and trastuzumab + pertuzumab over the course of several months and continually maintained in drug.

2020-01-26 | GSE121105 | GEO

Tumor region-specific microarray analysis according to trastuzumab distribution in breast cancer patient derived xenograft

Project description:Our novel drug imaging technique revealed that trastuzumab, which is representative antibody drug for breast and gastric cancer in clinical, distributed heterogeneously inside tumor even though its target receptor, HER2 (Human epidermal growth factor receptor 2) expressed homogeneously. For identifying a predominant regulator of trastuzumab tumor delivery in the tumor site, we tried tumor region-specific microarray analysis according to trastuzumab distribution in patient derived xenograft model.

2019-11-01 | GSE121787 | GEO

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