EGFR inhibition reverses epithelial‑mesenchymal transition, and decreases tamoxifen resistance via Snail and Twist downregulation in breast cancer cells
Open accessAbstract
Tamoxifen resistance remains a major obstacle in the treatment of estrogen receptor (ER)‑positive breast cancer. In recent years, the crucial role of the epithelial‑mesenchymal transition (EMT) process in the development of drug resistance in breast cancer has been underlined. However, the central molecules inducing the EMT process during the development of tamoxifen resistance remain to be elucidated. In the present study, it was demonstrated that tamoxifen‑resistant breast cancer cells underwent EMT and exhibited an enhanced cell motility and invasive behavior. The inhibition of snail family transcriptional repressor 1 (Snail) and twist family BHLH transcription factor 1 (Twist) reversed the EMT phenotype and decreased the tamoxifen resistance, migration and invasion of tamoxifen‑resistant breast cancer cells. In addition, it was observed that the inhibition of epidermal growth factor receptor (EGFR) reversed the EMT phenotype in tamoxifen‑resistant MCF7 (MCF‑7/TR) cells via the downregulation of Snail and Twist. Notably, the EGFR inhibitor, gefitinib, decreased tamoxifen resistance, migration and invasion through the inhibition of Snail and Twist. On the whole, the results of the present study suggest that EGFR may be a promising therapeutic target for tamoxifen‑resistant breast cancer. Moreover, it was suggested that gefitinib may serve as a potent novel therapeutic strategy for breast cancer patients, who have developed tamoxifen resistance.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Overexpression of epidermal growth factor receptor contributes to the development of tamoxifen-resistant breast cancer.
“Overexpression of epidermal growth factor receptor (EGFR), variations in TAM metabolism, and increased expression of drug-resistant proteins (P-glycoprotein, P-gp) all contribute to the development of TAM-resistant breast cancer.”
From Multifunctional and dual-targeting polymeric prodrug nanomicelles against tamoxifen-resistant breast cancer (2026) · cites this paper as [11]
The section on EGFR inhibition reports higher EGFR expression in tamoxifen-resistant MCF-7/TR cells than in MCF-7 cells, and the Discussion reports that an EGFR inhibitor decreased tamoxifen resistance. These findings support a role for EGFR, but the paper does not establish that EGFR overexpression causes the development of resistance. (LLM, conf=0.83)
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 67 · Cited by 17
- Authors
- Takeda, T., Tsubaki, M., Matsuda, T., Kimura, A., Jinushi, M., Obana, T., Takegami, M., & Nishida, S.
- Affiliations
- Kindai University (JP)
- Kindai University Hospital (JP)
- Venue
- Oncology Reports
- Publisher
- Spandidos Publications
- Published
- 2022-04-21
- Volume
- 47
- Issue
- 6
- ISSN
- 1021-335X (ISSN-L)
- 1791-2431
- OpenAlex
- W4224232800
- Cited by
- 17
- References
- 67
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 9 · 2023: 5
- FWCI
- 1.57
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Oncology Reports (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Japan Society for the Promotion of Science (20K16343)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
- Keywords
- EGFR inhibition, epithelial-mesenchymal transition, tamoxifen resistance, snails, Twist, estrogen receptor-positive breast cancer, gefitinib, cell migration, cell invasion, MCF-7 cells, therapeutic target
- MeSH terms
- Gefitinib, Breast Neoplasms, Female, Humans, Tamoxifen, Down-Regulation, Drug Resistance, Neoplasm, Cell Line, Tumor, Epithelial-Mesenchymal Transition, ErbB Receptors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
