ArticleFEBS open bio2017
ErbB2 signaling epigenetically suppresses microRNA-205 transcription via Ras/Raf/MEK/ERK pathway in breast cancer.
Article in FEBS open bio, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 26 citations in OpenAlex.
- Advances in the biological functions of miR‑205 in various diseases (Review).Molecular medicine reports · 2026Review
- Review
- Sp1 mechanotransduction regulates breast cancer cell invasion in engineered viscoelastic extracellular matrices.Biomaterials · 2026Article
- The molecular mechanisms and potential therapeutic implications of the crosstalk between DNA methylation and metabolic reprogramming in thyroid cancer.Cell death discovery · 2026Review
- Regulatory interplay of cyclin D1 and INSM1 in suppressing INSL6 expression: Implications for breast cancer biology.Biochemistry and biophysics reports · 2025Article
- Interaction of GPER-1 with the endocrine signaling axis in breast cancer.Frontiers in endocrinology · 2025Review
- miR-205-5p inhibits homocysteine-induced pulmonary microvascular endothelium dysfunction by targeting FOXO1.Acta biochimica et biophysica Sinica · 2023Article
- The Mechanism of DNA Methylation and miRNA in Breast Cancer.International journal of molecular sciences · 2023Review
- Nucleocytoplasmic transport of active HER2 causes fractional escape from the DCIS-like state.Nature communications · 2023Article
- Applying a Gene Reversal Rate Computational Methodology to Identify Drugs for a Rare Cancer: Inflammatory Breast Cancer.Cancer informatics · 2023Article
- miR-145, miR-205 and miR-451: potential tumor suppressors involved in the progression of in situ to invasive carcinoma of the breast.Breast cancer (Tokyo, Japan) · 2022Article
- Selective Extracellular Signal-Regulated Kinase 1/2 (ERK1/2) Inhibition by the SCH772984 Compound Attenuates In Vitro and In Vivo Inflammatory Responses and Prolongs Survival in Murine Sepsis Models.International journal of molecular sciences · 2021Article
- Epigenetic Regulation of Breast Cancer Stem Cells Contributing to Carcinogenesis and Therapeutic Implications.International journal of molecular sciences · 2021Review
- miR-34a-5p functions as a tumor suppressor in head and neck squamous cell cancer progression by targeting Flotillin-2.International journal of biological sciences · 2021Article
- miR-205 in Breast Cancer: State of the Art.International journal of molecular sciences · 2020Review
- The Therapeutic Potential of MicroRNAs in Cancer: Illusion or Opportunity?Pharmaceuticals (Basel, Switzerland) · 2020Review
- Unveiling the ups and downs of miR-205 in physiology and cancer: transcriptional and post-transcriptional mechanisms.Cell death & disease · 2020Review
- Regulation of breast cancer metastasis signaling by miRNAs.Cancer metastasis reviews · 2020Review
- MiR-205 Dysregulations in Breast Cancer: The Complexity and Opportunities.Non-coding RNA · 2019Review
- Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously reported that microRNA-205 (miR-205) is downregulated by overexpression of the receptor tyrosine kinase ErbB2 and that ectopic transfection of miR-205 precursor decreases ErbB2 tumorigenicity in soft agar. In this study, we further analyzed the regulatory mechanisms linking ErbB2 overexpression and miR-205 downregulation. In ErbB2-overexpressing breast epithelial cells, miR-205 expression was significantly increased by treatment with MEK inhibitor U0126 or PD98059, Raf-1 inhibitor ZM-336372, and ERK inhibitor SCH772984, but PI3K inhibitor LY294002 and p38 MAPK inhibitor SB203580 had no effect. We established breast epithelial cells overexpressing RafCAAX, a constitutively active form of Raf-1, and showed that overexpression of RafCAAX dramatically reduced miR-205 expression. In RafCAAX-overexpressing cells, miR-205 expression was also significantly increased by SCH772984. Moreover, miR-205 expression was significantly increased by treatment with DNA methyltransferase (DNMT) inhibitor 5-aza-2'-deoxycytidine and expression of several DNMT family members was increased in both ErbB2- and RafCAAX-overexpressing cells. DNA methylation analysis by bisulfite sequencing revealed that the putative miR-205 promoters were predominantly hypermethylated in both ErbB2- and RafCAAX-overexpressing cells. Reporter activity of the putative miR-205 promoters was reduced in both ErbB2-overexpressing and RafCAAX-overexpressing cells. Together, these findings indicate that ErbB2 signaling epigenetically suppresses miR-205 transcription via the Ras/Raf/MEK/ERK pathway.
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