ArticleBreast cancer research : BCR2018
SNAI2 upregulation is associated with an aggressive phenotype in fulvestrant-resistant breast cancer cells and is an indicator of poor response to endocrine therapy in estrogen receptor-positive metastatic breast cancer.
Article in Breast cancer research : BCR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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31 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Prognostic and clinicopathological value of Slug protein expression in breast cancer: a systematic review and meta-analysis.World journal of surgical oncology · 2022Pooled it
- RHAMM drives formation of polyploid cancer cells and confers resistance to ER-targeted therapy in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
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- Polyoxometalate inhibition of SOX2-mediated tamoxifen resistance in breast cancer.Cell communication and signaling : CCS · 2024Article
- Effect of quercetin on doxorubicin cytotoxicity in sensitive and resistant human MCF7 breast cancer cell lines.Biomedical reports · 2024Article
- Dynamic interplay of nuclear receptors in tumor cell plasticity and drug resistance: Shifting gears in malignant transformations and applications in cancer therapeutics.Cancer metastasis reviews · 2024Review
- INHBA is Enriched in HPV-negative Oropharyngeal Squamous Cell Carcinoma and Promotes Cancer Progression.Cancer research communications · 2024Article
- Upregulation of SLUG expression in canine mammary gland tumors and its prognostic significance.BMC veterinary research · 2023Article
- Transcriptome analysis of newly established carboplatin-resistant ovarian cancer cell model reveals genes shared by drug resistance and drug-induced EMT.British journal of cancer · 2023Article
- Review
- Transcriptome-Based Traits of Radioresistant Sublines of Non-Small Cell Lung Cancer Cells.International journal of molecular sciences · 2023Article
- Role of adenosine deaminase in prostate cancer progression.American journal of clinical and experimental urology · 2023Article
- Comprehensively prognostic and immunological analysis of snail family transcriptional repressor 2 in pan-cancer and identification in pancreatic carcinoma.Frontiers in immunology · 2023Article
- Estrone, the major postmenopausal estrogen, binds ERa to induce SNAI2, epithelial-to-mesenchymal transition, and ER+ breast cancer metastasis.Cell reports · 2022Article
- Deciphering the Role and Signaling Pathways of PKCα in Luminal A Breast Cancer Cells.International journal of molecular sciences · 2022Article
- PARP1-SNAI2 transcription axis drives resistance to PARP inhibitor, Talazoparib.Scientific reports · 2022Article
- MALAT1 as master regulator of biomarkers predictive of pan-cancer multi-drug resistance in the context of recalcitrant NRAS signaling pathway identified using systems-oriented approach.Scientific reports · 2022Article
- Potential roles of hsa_circ_000839 and hsa_circ_0005986 in breast cancer.Journal of clinical laboratory analysis · 2022Article
- Sustained compensatory p38 MAPK signaling following treatment with MAPK inhibitors induces the immunosuppressive protein CD73 in cancer: combined targeting could improve outcomes.Molecular oncology · 2021Article
- Endocrine resistance in breast cancer: from molecular mechanisms to therapeutic strategies.Journal of molecular medicine (Berlin, Germany) · 2021Review
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5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundEndocrine resistance in estrogen receptor-positive (ER+) breast cancer is a major clinical problem and is associated with accelerated cancer cell growth, increased motility and acquisition of mesenchymal characteristics. However, the specific molecules and pathways involved in these altered features remain to be detailed, and may be promising therapeutic targets to overcome endocrine resistance.
methodsIn the present study, we evaluated altered expression of epithelial-mesenchymal transition (EMT) regulators in ER+ breast cancer cell models of tamoxifen or fulvestrant resistance, by gene expression profiling. We investigated the specific role of increased SNAI2 expression in fulvestrant-resistant cells by gene knockdown and treatment with a SNAIL-p53 binding inhibitor, and evaluated the effect on cell growth, migration and expression of EMT markers. Furthermore, we evaluated SNAI2 expression by immunohistochemical analysis in metastatic samples from two cohorts of patients with breast cancer treated with endocrine therapy in the advanced setting.
resultsSNAI2 was found to be significantly upregulated in all endocrine-resistant cells compared to parental cell lines, while no changes were observed in the expression of other EMT-associated transcription factors. SNAI2 knockdown with specific small interfering RNA (siRNA) converted the mesenchymal-like fulvestrant-resistant cells into an epithelial-like phenotype and reduced cell motility. Furthermore, inhibition of SNAI2 with specific siRNA or a SNAIL-p53 binding inhibitor reduced growth of cells resistant to fulvestrant treatment. Clinical evaluation of SNAI2 expression in two independent cohorts of patients with ER+ metastatic breast cancer treated with endocrine therapy in the advanced setting (N = 86 and N = 67) showed that high SNAI2 expression in the metastasis correlated significantly with shorter progression-free survival on endocrine treatment (p = 0.0003 and p = 0.004).
conclusionsOur results suggest that SNAI2 is a key regulator of the aggressive phenotype observed in endocrine-resistant breast cancer cells, an independent prognostic biomarker in ER+ advanced breast cancer treated with endocrine therapy, and may be a promising therapeutic target in combination with endocrine therapies in ER+ metastatic breast cancer exhibiting high SNAI2 levels.
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