ArticleMolecular oncology2014
HER2 mediated de novo production of TGFβ leads to SNAIL driven epithelial-to-mesenchymal transition and metastasis of breast cancer.
Article in Molecular oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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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.
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Who cites it
51 citing papers in PubMed, 68 citations in OpenAlex.
- Interleukin-34-Induced Arg1+ Macrophages Play a Key Role in Breast Cancer Brain Metastasis.Cancer research communications · 2026Article
- Preclinical models of breast cancer metastasis: strengths, limitations, and clinical relevance.NPJ breast cancer · 2026Review
- ERBB2 amplification is a late event in the pathogenesis of high-grade endometrial carcinomas with heterogeneous HER2 expression.The Journal of pathology · 2026Article
- Effects of Eribulin on Epithelial-Mesenchymal Plasticity in Patient-Derived Breast Cancer Cultures and Excised Tissues.Cancers · 2026Article
- Review
- Biological profile of breast cancer brain metastasis.Acta neuropathologica communications · 2025Review
- Association Between Human Epidermal Growth Factor Receptor 2-Low Status and Time to Development of Brain Metastases Among Patients With Breast Cancer: A Retrospective Cohort Study.JCO precision oncology · 2025Article
- Comprehensive molecular interaction map of TGFβ induced epithelial to mesenchymal transition in breast cancer.NPJ systems biology and applications · 2024Article
- Biology of breast cancer brain metastases and novel therapies targeting the blood brain barrier: an updated review.Medical oncology (Northwood, London, England) · 2023Review
- The Journey of Cancer Cells to the Brain: Challenges and Opportunities.International journal of molecular sciences · 2023Review
- AKT-driven epithelial-mesenchymal transition is affected by copper bioavailability in HER2 negative breast cancer cells via a LOXL2-independent mechanism.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- The super-enhancer repertoire in porcine liver.Journal of animal science · 2023Article
- Review
- Article
- Beyond Genetics: Metastasis as an Adaptive Response in Breast Cancer.International journal of molecular sciences · 2022Review
- HER2-positive breast cancer brain metastasis: A new and exciting landscape.Cancer reports (Hoboken, N.J.) · 2022Review
- HER2-low breast cancer could be associated with an increased risk of brain metastasis.International journal of clinical oncology · 2022Article
- Inhibition of the proliferation, invasion, migration, and epithelial-mesenchymal transition of prostate cancer cells through the action ofTranslational andrology and urology · 2022Article
- Identification of potential genes related to breast cancer brain metastasis in breast cancer patients.Bioscience reports · 2021Article
- Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
HER2 is an important determinant of poor prognosis in breast cancer patients. Studies indicate that HER2 positive tumors are mostly resistant to therapy and have high metastatic potential however, the underlying mechanisms remain unknown. In this study, MDA-MB-231 and MCF-7 breast cancer cells with their HER2 overexpressing syngeneic variants were used to delineate the role of HER2 in EMT and metastasis. Our results demonstrated that HER2 overexpression increased the invasive potential of cells. Our results also showed that HER2 overexpression lead to the production of TGFβ resulting in the activation of TGFβ/SMAD signaling. Furthermore, activation of SNAIL, SLUG and ZEB-1, the transcriptional repressors of E-cadherin and increased mesenchymal characteristics were observed in high HER2 cells. Interestingly, EMT by HER2 was mediated through TGFβ. Intravenous injection of high HER2 MDA-MB-231 (HH) cells in athymic nude mice showed early and substantial metastasis as compared to the parent cells establishing the direct role of HER2 in metastasis. Our results showed that inhibition of HER2 mediated EMT by cucurbitacin B a triterpenoid, resulted in the suppression of brain metastasis of breast cancer cells. Taken together, our results identify a novel mechanism of HER2 in promoting breast cancer metastasis through de novo synthesis of TGFβ leading to EMT, an initial and essential step of metastasis.
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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.