ArticleCancer medicine2017
Protein lysine methyltransferase SMYD3 is involved in tumorigenesis through regulation of HER2 homodimerization.
Article in Cancer medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Canonical and Non-Canonical Functions of Histone H3K4 Methylation Modifiers in Cancer.Cancer science · 2025Review
- Bifaceted functions of histone methyltransferases.Epigenomics · 2025Article
- Direct lysine dimethylation of IRF3 by the methyltransferase SMYD3 attenuates antiviral innate immunity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- SMYD3 drives cell cycle and epithelial-mesenchymal transition pathways through dual gene transcriptional repression and activation in HPV-negative head and neck cancer.Scientific reports · 2025Article
- SMYD family in cancer: epigenetic regulation and molecular mechanisms of cancer proliferation, metastasis, and drug resistance.Experimental & molecular medicine · 2024Review
- The impact of nitric oxide on HER family post-translational modification and downstream signaling in cancer.Frontiers in physiology · 2024Review
- [Research Progress of Role and Mechanism of SETD7 in Tumor Occurrence and Progression].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2023Article
- HNMT Upregulation Induces Cancer Stem Cell Formation and Confers Protection against Oxidative Stress through Interaction with HER2 in Non-Small-Cell Lung Cancer.International journal of molecular sciences · 2022Article
- Identifying novel SMYD3 interactors on the trail of cancer hallmarks.Computational and structural biotechnology journal · 2022Article
- Playing on the Dark Side: SMYD3 Acts as a Cancer Genome Keeper in Gastrointestinal Malignancies.Cancers · 2021Review
- Mechanism of the Conformational Change of the Protein Methyltransferase SMYD3: A Molecular Dynamics Simulation Study.International journal of molecular sciences · 2021Article
- SMYD3: a regulator of epigenetic and signaling pathways in cancer.Clinical epigenetics · 2021Review
- Application of Artificial Intelligence Technology in Oncology: Towards the Establishment of Precision Medicine.Cancers · 2020Review
- Targeting SMYD3 to Sensitize Homologous Recombination-Proficient Tumors to PARP-Mediated Synthetic Lethality.iScience · 2020Article
- Review
- Amplified fluorescence imaging of HER2 dimerization on cancer cells by using a co-localization triggered DNA nanoassembly.Mikrochimica acta · 2019Article
- SMYD3 promotes the epithelial-mesenchymal transition in breast cancer.Nucleic acids research · 2019Article
- Host factor SMYD3 is recruited by Ebola virus nucleoprotein to facilitate viral mRNA transcription.Emerging microbes & infections · 2019Article
- Identification of potential key protein interaction networks of BK virus nephropathy in patients receiving kidney transplantation.Scientific reports · 2018Article
- LCK as a Potential Therapeutic Target for Acute Rejection after Kidney Transplantation: A Bioinformatics Clue.Journal of immunology research · 2018Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HER2 is a receptor tyrosine kinase, which is amplified and overexpressed in a subset of human cancers including breast and gastric cancers, and is indicated in its involvement in progression of cancer. Although its specific ligand(s) has not been detected, HER2 homodimerization, which is critical for its activation, is considered to be dependent on its expression levels. Here, we demonstrate a significant role of HER2 methylation by protein lysine methyltransferase SMYD3 in HER2 homodimerization. We found that SMYD3 trimethylates HER2 protein at lysine 175. HER2 homodimerization was enhanced in the presence of SMYD3, and substitution of lysine 175 of HER2 with alanine (HER2-K175A) reduced the formation of HER2 homodimers. Furthermore, HER2-K175A revealed lower level of autophosphorylation than wild-type HER2. We also identified that knockdown of SMYD3 attenuated this autophosphorylation in breast cancer cells. Our results imply that SMYD3-mediated methylation of HER2 at Lysine 175 may regulate the formation of HER2 homodimer and subsequent autophosphorylation and suggest that the SMYD3-mediated methylation pathway seems to be a good target for development of novel anti-cancer therapy.
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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.