ArticleAnticancer research2017
ESE-1 Knockdown Attenuates Growth in Trastuzumab-resistant HER2
Article in Anticancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Hypoxia-induced ELF3 promotes tumor angiogenesis through IGF1/IGF1R.EMBO reports · 2022Article
- E74-like factor 3 suppresses microRNA-485-5p transcription to trigger growth and metastasis of ovarian cancer cells with the involvement of CLDN4/Wnt/β-catenin axis.Saudi journal of biological sciences · 2021Article
- Ultrasound-mediated delivery of siESE complexed with microbubbles attenuates HER2+/- cell line proliferation and tumor growth in rodent models of breast cancer.Nanotheranostics · 2019Article
- ELF3, ELF5, EHF and SPDEF Transcription Factors in Tissue Homeostasis and Cancer.Molecules (Basel, Switzerland) · 2018Review
- LMO4 mediates trastuzumab resistance in HER2 positive breast cancer cells.American journal of cancer research · 2018Article
- Evaluation of the Insulin-like Growth Factor Receptor Pathway in Patients with Advanced Breast Cancer Treated with Trastuzumab.Cancer genomics & proteomicsArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND/
aimESE-1/Elf3 controls transformation properties in mammary epithelial cells, and is most clinically relevant in HER2 MATERIALS AND
methodsWe used cell proliferation, clonogenicity, viability, and soft agar assays to measure the effects of ESE-1 knockdown in cell lines.
resultsESE-1 knockdown in the resistant cell lines inhibited HER2 and other downstream effectors in a cell-type specific manner, but caused down-regulation of pAkt and cyclin D1 in both sublines. In parental BT474 and SKBR3 ESE-1 silencing revealed a potent anti-proliferative effect that mimics the trastuzumab-mediated growth inhibition but did not enhance trastuzumab sensitivity in the resistant sublines.
conclusionThis study provides rationale to study ESE-1 as a novel mean to treat HER2
Indexed as
Identifiers
What OpenQuestion holds
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.