Knockdown of SMYD3 by RNA interference down-regulates c-Met expression and inhibits cells migration and invasion induced by HGF

Zou, Jianing; Wang, Shuzhen; Yang, Jia-Sen; Luo, Xue‐Gang; Xie, Jinghang; Xi, Tao

doi:10.1016/j.canlet.2009.02.015

Cited by 55 publications

(49 citation statements)

References 33 publications

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“…Remarkably, higher SMYD3 transcript levels were associated with locally advanced disease, suggesting an association with more aggressive PCa. Interestingly, SMYD3 overexpression has been linked with enhanced proliferation and loss of differentiation (Hamamoto et al 2006, Wang et al 2008, Zou et al 2009, Ren et al 2011 and this may support the association found in PCa. Moreover, SMYD3 also methylates H4K5 and H4K20 and other non-histone proteins, which may also contribute to its oncogenic role (Foreman et al 2011, Van Aller et al 2012.…”

Section: Discussionsupporting

confidence: 67%

Deregulated expression of selected histone methylases and demethylases in prostate carcinoma

Vieira¹,

Costa-Pinheiro²,

Ramalho-Carvalho³

et al. 2013

Endocrine-Related Cancer

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Prostate cancer (PCa), a leading cause of cancer-related morbidity and mortality, arises through the acquisition of genetic and epigenetic alterations. Deregulation of histone methyltransferases (HMTs) or demethylases (HDMs) has been associated with PCa development and progression. However, the precise influence of altered HMTs or HDMs expression and respective histone marks in PCa onset and progression remains largely unknown. To clarify the role of HMTs and HDMs in prostate carcinogenesis, expression levels of 37 HMTs and 20 HDMs were assessed in normal prostate and PCa tissue samples by RT-qPCR. SMYD3, SUV39H2, PRMT6, KDM5A, and KDM6A were upregulated, whereas KMT2A-E (MLL1-5) and KDM4B were downregulated in PCa, compared with normal prostate tissues. Remarkably, PRMT6 was the histone modifier that best discriminated normal from tumorous tissue samples. Interestingly, EZH2 and SMYD3 expression levels significantly correlated with less differentiated and more aggressive tumors. Remarkably, SMYD3 expression levels were of independent prognostic value for the prediction of disease-specific survival of PCa patients with clinically localized disease submitted to radical prostatectomy. We concluded that expression profiling of HMTs and HDMs, especially SMYD3, might be of clinical usefulness for the assessment of PCa patients and assist in pre-therapeutic decision-making.

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Section: Discussionsupporting

confidence: 67%

Deregulated expression of selected histone methylases and demethylases in prostate carcinoma

Vieira¹,

Costa-Pinheiro²,

Ramalho-Carvalho³

et al. 2013

Endocrine-Related Cancer

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“…SMYD3 is also involved in apoptosis and the inhibition of cell growth, migration, and invasion (Xu et al 2006, Zou et al 2009). In the present paper, we observed Smyd3 mRNA expression patterns and protein localization during mouse preimplantation development and showed that Smyd3 knockdown led to a defect in the ability of Smyd3 mRNA to attach to a matrix and outgrowth in vitro and to a reduction in the number of viable offspring, which suggests that SMYD3 plays important roles during peri-implantation development.…”

Section: Discussionmentioning

confidence: 99%

“…Evidence has accumulated that suggests that SMYD3 recruits RNA polymerase II through an RNA helicase to form a transcription complex and that it elicits its oncogenic effects by activating the transcription of downstream target genes (Hamamoto et al 2004, 2006, Liu et al 2007. Previous reports have demonstrated that enhanced expression of SMYD3 is essential for the growth of human cancer cells (Hamamoto et al 2004(Hamamoto et al , 2006, whereas the suppression of SMYD3 expression leads to apoptosis and the inhibition of cell growth, migration, and invasion (Chen et al 2007, Zou et al 2009). Recent studies have determined that Smyd3 plays an important role in the development of heart and skeletal muscle during zebrafish embryogenesis (Fujii et al 2011).…”

Section: Introductionmentioning

confidence: 99%

Histone methyltransferase Smyd3 regulates early embryonic lineage commitment in mice

Suzuki¹,

Nozawa²,

Tsukamoto³

et al. 2015

Reproduction

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SET and MYND domain-containing protein 3 (Smyd3) is a histone H3 lysine 4 (H3K4) di-and tri-methyltransferase that forms a transcriptional complex with RNA polymerase II and activates the transcription of oncogenes and cell cycle genes in human cancer cells. However, the study of Smyd3 in mammalian early embryonic development has not yet been addressed. In the present study, we investigated the expression pattern of Smyd3 in mouse preimplantation embryos and the effects of RNA interference (RNAi)-mediated Smyd3 repression on the development of mouse embryos. We showed that Smyd3 mRNA levels increased after the two-cell stage, peaked at the four-cell stage, and gradually decreased thereafter. Moreover, in two-cell to eight-cell embryos, SMYD3 staining was more intense in the nuclei than it was in the cytoplasm. In Smyd3-knockdown embryos, the percentage of inner cell mass (ICM)-derived colony formation and trophectoderm (TE)-derived cell attachment were significantly decreased, which resulted in a reduction in the number of viable offspring. Furthermore, the expression of Oct4 and Cdx2 during mid-preimplantation gene activation was significantly decreased in Smyd3-knockdown embryos. In addition, the transcription levels of ICM and epiblast markers, such as Oct4, Nanog, and Sox2, the transcription levels of primitive endoderm markers, such as Gata6, and the transcription levels of TE markers, such as Cdx2 and Eomes, were significantly decreased in Smyd3-knockdown blastocysts. These findings indicate that SMYD3 plays an important role in early embryonic lineage commitment and peri-implantation development through the activation of lineage-specific genes.Reproduction (2015) 150 21-30

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“…SMYD3 is a novel SET-domain-containing lysine histone methyltransferase which has been regarded as an important factor in carcinogenesis. Formed a complex with RNA polymerase II through an interaction with the RNA helicase HELZ, SMYD3 specifically methylates H3K4 and activates the transcription of a set of downstream genes (including of Nkx2.8, hTERT, WNT10B, VEGFR1, c-Met, etc) containing a ''5′ -CCCTCC -3′" or "5′ -GGAGGG -3" sequence in the promoter region (Fig 6) (Hamamoto et al, 2004;Hamamoto et al, 2006;Kunizaki et al, 2007;Zou et al, 2009). It seems that the N-terminal region of SMYD3 plays an important role for the regulation of its methyltransferase activity, and the cleavage of 34 amino acids in the N-terminal region or interaction with heat shock protein 90 alpha (HSP90α) may enhance the histone methyltransferase (HMTase) activity compared to the full-length protein (Silva et al, 2008).…”

Section: Histone Lysine Methyltransferase (Hkmts)mentioning

confidence: 99%

“…It seems that the N-terminal region of SMYD3 plays an important role for the regulation of its methyltransferase activity, and the cleavage of 34 amino acids in the N-terminal region or interaction with heat shock protein 90 alpha (HSP90α) may enhance the histone methyltransferase (HMTase) activity compared to the full-length protein (Silva et al, 2008). Enhanced expression of SMYD3 is essential for the growth of many cancer cells (such as breast cancer, colorectal carcinoma, hepatocellular carcinoma, etc), and it also could stimulate cell adhesion and migration, whereas suppression of SMYD3 by RNAi or other reagents induces apoptosis and inhibits cell proliferation and migration (Hamamoto et al, 2004;Hamamoto et al, 2006;Luo et al, 2007;Wang et al, 2008;Luo et al, 2009;Zou et al, 2009;Luo et al, 2010). SMYD3 may be an important coactivator of estrogen receptor (ER) in the estrogen signal pathway.…”

Section: Histone Lysine Methyltransferase (Hkmts)mentioning

confidence: 99%

Histone Modification and Breast Cancer

Luo¹,

Guo²,

Guo³

et al. 2011

Breast Cancer - Focusing Tumor Microenvironment, Stem Cells and Metastasis

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Knockdown of SMYD3 by RNA interference down-regulates c-Met expression and inhibits cells migration and invasion induced by HGF

Cited by 55 publications

References 33 publications

Deregulated expression of selected histone methylases and demethylases in prostate carcinoma

Deregulated expression of selected histone methylases and demethylases in prostate carcinoma

Histone methyltransferase Smyd3 regulates early embryonic lineage commitment in mice

Histone Modification and Breast Cancer

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