ArticleMolecular cancer2010
EGFR isoforms and gene regulation in human endometrial cancer cells.
Article in Molecular cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 55 citations in OpenAlex.
- A phase II evaluation of gefitinib in the treatment of persistent or recurrent endometrial cancer: a Gynecologic Oncology Group study.Gynecologic oncology · 2013Trial
- Lapatinib and potential prognostic value of EGFR mutations in a Gynecologic Oncology Group phase II trial of persistent or recurrent endometrial cancer.Gynecologic oncology · 2012Trial
- Isoforms in action: The impact of transcript diversity in phenotype.Genetics and molecular biology · 2026Article
- Article
- Interpretation of Epidermal Growth Factor Receptor Status in Microscopic Tumor-Free Surgical Margins and Lymph Nodes in Patients with Oral Squamous Cell Carcinoma: An Analysis of 125 Margins.Journal of maxillofacial and oral surgery · 2024Article
- Cell migration and proliferation capacity of IPEC-J2 cells after short-chain fatty acid exposure.PloS one · 2024Article
- COVID-19-The Shift of Homeostasis into Oncopathology or Chronic Fibrosis in Terms of Female Reproductive System Involvement.International journal of molecular sciences · 2023Review
- Incorporating the epidermal growth factor receptor expression and histopathological parameters in a mathematical model to predict the prognosis of oral squamous cell carcinoma: a prospective observational cohort study.Journal of maxillofacial and oral surgery · 2022Article
- EGFR blocker lapatinib inhibits the synthesis of matrix metalloproteinases from synovial fibroblasts.Turkish journal of medical sciences · 2022Article
- Endothelial cell-specific molecule 1 (ESM1) promoted by transcription factor SPI1 acts as an oncogene to modulate the malignant phenotype of endometrial cancer.Open medicine (Warsaw, Poland) · 2022Article
- Exploration of the Effect and Potential Mechanism of Echinacoside Against Endometrial Cancer Based on Network Pharmacology and in vitro Experimental Verification.Drug design, development and therapy · 2022Article
- Evaluation of the Differences in the Expression of Biogenic Amine-Related mRNAs and Proteins in Endometrioid Endometrial Cancer.Journal of clinical medicine · 2021Article
- Review
- Xmrks the Spot: Fish Models for Investigating Epidermal Growth Factor Receptor Signaling in Cancer Research.Cells · 2021Review
- In silico analysis of alternative splicing on drug-target gene interactions.Scientific reports · 2020Article
- Long noncoding RNA EGFR-AS1 promotes cell growth and metastasis via affecting HuR mediated mRNA stability of EGFR in renal cancer.Cell death & disease · 2019Article
- A link between a synonymous SNP and the clinical response to tyrosine kinase inhibitors.Non-coding RNA investigation · 2018Article
- Long noncoding RNA EGFR-AS1 mediates epidermal growth factor receptor addiction and modulates treatment response in squamous cell carcinoma.Nature medicine · 2017Article
- Domain-based prediction of the human isoform interactome provides insights into the functional impact of alternative splicing.PLoS computational biology · 2017Article
- Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundEpidermal growth factor (EGF) and its receptor (EGFR) constitute a principal growth-promoting pathway in endometrial cancer cells. Pre-clinical studies were undertaken to compare the expression of EGFR isoforms and the downstream effects of activating or blocking EGFR function in Ishikawa H cells, derived from a moderately differentiated type I endometrioid adenocarcinoma, or in Hec50co cells, derived from a poorly differentiated type II adenocarcinoma with papillary serous sub-differentiation.
resultsWe investigated whether EGFR mutations are present in the tyrosine kinase domain (exons 18-22) of EGFR and also whether EGFR isoforms are expressed in the Ishikawa H or Hec50co cell lines. Sequence of the EGFR tyrosine kinase domain proved to be wild type in both cell lines. While both cell lines expressed full-length EGFR (isoform A), EGFR and sEGFR (isoform D) were expressed at significantly lower levels in Hec50co cells compared to Ishikawa H cells. Analysis of gene expression following EGF vs. gefitinib treatment (a small molecule EGFR tyrosine kinase inhibitor) was performed. Early growth response 1, sphingosine kinase 2, dual specificity phosphatase 6, and glucocorticoid receptor DNA binding factor 1 are members of a cluster of genes downstream of EGFR that are differentially regulated by treatment with EGF compared to gefitinib in Ishikawa H cells, but not in Hec50co cells.
conclusionsType I Ishikawa H and type II Hec50co endometrial carcinoma cells both express EGFR and sEGFR, but differ markedly in their responsiveness to the EGFR inhibitor gefitinib. This difference is paralleled by differences in the expression of sEGFR and EGFR, as well as in their transcriptional response following treatment with either EGF or gefitinib. The small cluster of differently regulated genes reported here in these type I vs. type II endometrial cancer-derived cell lines may identify candidate biomarkers useful for predicting sensitivity to EGFR blockade.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.