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Smyd3 is a transcriptional potentiator of multiple cancer-promoting genes and required for liver or colon cancer development

ABSTRACT: Smyd3 is a histone methyltransferase implicated in tumorigenesis. Here we show that Smyd3 expression in mice is required but not sufficient for chemically induced liver and colon cancer formation. In these organs Smyd3 is functioning in the nucleus as a direct transcriptional activator of several key genes involved in cell proliferation, epithelial-mesenchymal transition, JAK/Stat3 oncogenic pathways, as well as of the c-myc and b-catenin oncogenes. Smyd3 specifically interacts with H3K4Me3-modified histone tails and is recruited to the core promoter regions of many but not all active genes. Smyd3 binding density on target genes positively correlates with increased RNA Pol-II density and transcriptional outputs. The results suggest that Smyd3 is an essential transcriptional potentiator of a multitude of cancer-related genes.

ORGANISM(S): Mus musculus

PROVIDER: GSE67790 | GEO | 2016/01/01

SECONDARY ACCESSION(S): PRJNA280944

REPOSITORIES: GEO

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Project description:SET (Su) and MYND (myeloid-Nervy-DEAF-1) domain-containing protein (SMYD) is a methyltransferase family, including five members of which SMYD1, SMYD2, SMYD3 and SMYD4, has been found to play critical roles in human carcinogenesis. It has been demonstrated that the altered expression of SMYD3 is associated with the progression of several solid tumors, including bladder cancer, glioma, gastric cancer, prostate cancer and colorectal cancer. Several trials have explored the effects of SMYD3 overexpression on proliferation, viability, cancer cells migration and invasion. The series of elegant experiments suggested that SMYD3 could serve as a potential biomarker for clinically aggressive disease and an attractive therapeutic target. In our previous study (PMID: 26980013), we found SMYD3 expression is frequently upregulated in human esophageal squamous cell carcinoma (ESCC) clinical tissues, correlating with overall survival of ESCC patients. RNAi-mediated knockdown of SMYD3 suppressed ESCC cell proliferation, migration and invasion in vitro, and inhibited local tumor invasion in vivo. To identify genes and biological pathways associated with SMYD3 functions and mechanism, SMYD3 was knockdowned bypGLV3/H1/GFP/+Puro Vector in ESCC cell line KYSE150 with an empty plasmid as a control, these two cells were applied for mRNA expression profile analyses to find the differentially expressed genes using GeneChipÂ® PrimeViewâ¢ Human Gene Expression Array. shRNA sequences targeting SMYD3 was ligated into the pGLV3/H1/GFP/+Puro Vector and transfected into ESCC cell line KYSE150 with an empty plasmid as a control. The mRNA expression profiles of SMYD3 knockdown was analyzed by GeneChipÂ®Â PrimeViewâ¢Â HumanÂ Gene Expression Array (Affymetrix,Â USA). The knockdown of SMYD3 was confirmed by QRT-PCR and Western blot. Total RNAs from SMYD3 knockdown cells and control cells were extracted for GeneChipÂ® PrimeViewâ¢ Human Gene Expression Array.

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Smyd3 is a transcriptional potentiator of multiple cancer-promoting genes and required for liver or colon cancer development

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