Disease relevance of SMYD3

• We previously reported that upregulation of SMYD3, a histone methyltransferase, promoted cell growth in human colorectal and hepatocellular carcinomas [1].
• Variable number of tandem repeats polymorphism in the SMYD3 promoter region and the risk of familial breast cancer [2].
• We previously reported that upregulation of SMYD3, a histone H3 lysine-4-specific methyltransferase, plays a key role in the proliferation of colorectal carcinoma (CRC) and hepatocellular carcinoma (HCC) [3].
• Our results identify SMYD3 as a new coactivator for ER-mediated transcription, providing a possible link between SMYD3 overexpression and breast cancer [4].

High impact information on SMYD3

• These data suggest that the common variable number of tandem repeats polymorphism in SMYD3 is a susceptibility factor for some types of human cancer [1].
• A variable number of tandem repeats polymorphism in an E2F-1 binding element in the 5' flanking region of SMYD3 is a risk factor for human cancers [1].
• 8. The SET domain of SMYD3 showed histone H3-lysine 4 (H3-K4)-specific methyltransferase activity, which was enhanced in the presence of the heat-shock protein HSP90A [5].
• Introduction of SMYD3 into NIH3T3 cells enhanced cell growth, whereas genetic knockdown with small-interfering RNAs (siRNAs) in cancer cells resulted in significant growth suppression [5].
• Here we report the identification of SMYD3, a gene that is over-expressed in the majority of colorectal carcinomas and hepatocellular carcinomas [5].

Biological context of SMYD3

• SMYD3-NY, a novel SMYD3 mRNA transcript variant, may have a role in human spermatogenesis [6].
• Moreover, we show here that SMYD3 could promote breast carcinogenesis by directly regulating expression of the proto-oncogene WNT10B [3].

Anatomical context of SMYD3

• In this study, a novel SMYD3 transcript variant, termed SMYD3-NY (GenBank Accession No. AY186742), was identified by hybridization of adult and fetal human testis cDNA probes with a human cDNA microarray [6].

Other interactions of SMYD3

• In the present study, we show that SET and MYND domain-containing protein 3 (SMYD3), a histone methyltransferase implicated in oncogenesis, directly trans-activates the telomerase reverse transcriptase (hTERT) gene that is essential for cellular immortalization and transformation [7].
• Our findings suggest that SMYD3 has histone methyltransferase activity and plays an important role in transcriptional regulation as a member of an RNA polymerase complex [5].

References