ArticleExperimental and therapeutic medicine2020
SMYD3 promotes colon adenocarcinoma (COAD) progression by mediating cell proliferation and apoptosis.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 10 citations in OpenAlex.
- Molecular Basis of Simalikalactone D Sensitivity in Triple-Negative Breast Cancer Cells.Biomolecules · 2025Article
- SMYD family in cancer: epigenetic regulation and molecular mechanisms of cancer proliferation, metastasis, and drug resistance.Experimental & molecular medicine · 2024Review
- Zinc finger myeloid Nervy DEAF-1 type (ZMYND) domain containing proteins exert molecular interactions to implicate in carcinogenesis.Discover oncology · 2022Review
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Authors and funding
7 authors at 1 institution in 1 country.
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Abstract
Colon adenocarcinoma (COAD) is a type of common malignant tumor originating in the digestive tract. Recently, targeted therapy has had significant effects on the treatment of COAD. However, more effective molecular targets need to be developed. SET and MYND domain-containing protein 3 (SMYD3) is a type of methyltransferase which methylates histone and non-histone proteins. The effects of SMYD3 on cancer progression and metastasis have been widely revealed. However, its possible role in COAD remains unclear. The current study demonstrated that SMYD3 expression was upregulated in human COAD tissues via analyzing the The Cancer Genome Atlas (TCGA) database and the immunohistochemical assays. Furthermore, the expression of SMYD3 was correlated with prognosis and tumor stage (P=0.038) in patients with COAD. Colony formation, MTT, FCM assays and animal assays indicated SMYD3 affected the proliferation, apoptosis and the cell cycle of COAD cells
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