ArticleOncotarget2015
SMYD3 contributes to a more aggressive phenotype of prostate cancer and targets Cyclin D2 through H4K20me3.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 76 citations in OpenAlex.
- Review
- Epigenetic insights into prostate cancer: exploring histone modifications and their therapeutic implications.Frontiers in oncology · 2025Review
- The KDM5 inhibitor PBIT reduces proliferation of castration-resistant prostate cancer cells via cell cycle arrest and the induction of senescence.Experimental cell research · 2024Article
- Smyd3 negatively regulates the anti-viral pathway by promoting TAK1 degradation in teleost fish.Journal of virology · 2023Article
- The SMYD3-MAP3K2 signaling axis promotes tumor aggressiveness and metastasis in prostate cancer.Science advances · 2023Article
- SMYD3 drives the proliferation in gastric cancer cells via reducing EMP1 expression in an H4K20me3-dependent manner.Cell death & disease · 2023Article
- Review
- Histone 4 lysine 20 tri-methylation: a key epigenetic regulator in chromatin structure and disease.Frontiers in genetics · 2023Review
- H3 histone methylation landscape in male urogenital cancers: from molecular mechanisms to epigenetic biomarkers and therapeutic targets.Frontiers in cell and developmental biology · 2023Review
- Construction of DNA methylation-based nomogram for predicting biochemical-recurrence-free survival in prostate cancer.Medicine · 2022Article
- SMYD3 promotes aerobic glycolysis in diffuse large B-cell lymphoma via H3K4me3-mediated PKM2 transcription.Cell death & disease · 2022Article
- Oleocanthal Attenuates Metastatic Castration-Resistant Prostate Cancer Progression and Recurrence by Targeting SMYD2.Cancers · 2022Article
- SMYD3 promotes hepatocellular carcinoma progression by methylating S1PR1 promoters.Cell death & disease · 2021Article
- Mechanism of the Conformational Change of the Protein Methyltransferase SMYD3: A Molecular Dynamics Simulation Study.International journal of molecular sciences · 2021Article
- Review
- Epigenetic mechanisms underlying prostate cancer radioresistance.Clinical epigenetics · 2021Review
- Article
- Analysis of SET and MYND Domain-Containing Protein 3 (SMYD3) Expression in Gallbladder Cancer: a Pilot Study.Indian journal of surgical oncology · 2021Article
- SMYD3: a regulator of epigenetic and signaling pathways in cancer.Clinical epigenetics · 2021Review
- Methylation of histone 4's lysine 20: a critical analysis of the state of the field.Physiological genomics · 2021Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer (PCa) is one of the most incident cancers worldwide but clinical and pathological parameters have limited ability to discriminate between clinically significant and indolent PCa. Altered expression of histone methyltransferases and histone methylation patterns are involved in prostate carcinogenesis. SMYD3 transcript levels have prognostic value and discriminate among PCa with different clinical aggressiveness, so we decided to investigate its putative oncogenic role on PCa.We silenced SMYD3 and assess its impact through in vitro (cell viability, cell cycle, apoptosis, migration, invasion assays) and in vivo (tumor formation, angiogenesis). We evaluated SET domain's impact in PCa cells' phenotype. Histone marks deposition on SMYD3 putative target genes was assessed by ChIP analysis.Knockdown of SMYD3 attenuated malignant phenotype of LNCaP and PC3 cell lines. Deletions affecting the SET domain showed phenotypic impact similar to SMYD3 silencing, suggesting that tumorigenic effect is mediated through its histone methyltransferase activity. Moreover, CCND2 was identified as a putative target gene for SMYD3 transcriptional regulation, through trimethylation of H4K20.Our results support a proto-oncogenic role for SMYD3 in prostate carcinogenesis, mainly due to its methyltransferase enzymatic activity. Thus, SMYD3 overexpression is a potential biomarker for clinically aggressive disease and an attractive therapeutic target in PCa.
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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.