Rabbit Anti-Human Histone H4 (Acetyl-Lys8) polyclonal antibody

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 in vitro and promoted tumor growth in mice in vivo. In summary, the results demonstrated the effects of SMYD3 on COAD progression and we hypothesized that SMYD3 is a novel molecular target for COAD treatment.

We have recently shown that histone deacetylase 6 (HDAC6) is critically involved in the pathogenesis of acute kidney injury. Its role in renal fibrosis, however, remains unclear. In this study, we examined the effect of ricolinostat (ACY-1215), a selective inhibitor of HDAC6, on the development of renal fibrosis in a murine model induced by unilateral ureteral obstruction (UUO). HDAC6 was highly expressed in the kidney following UUO injury, which was coincident with deposition of collagen fibrils and expression of alpha-smooth muscle actin, libronectin, and collagen type III. Administration of ACY-1215 reduced these fibrotic changes and inhibited UUO-induced expression of transforming growth factor-beta 1 and phosphorylation of Smad3 while increasing expression of Smad7. ACY-1215 treatment also suppressed phosphorylation of epidermal growth factor receptor (EGFR) and several signaling molecules associated with renal fibrogenesis, including AKT, STAT3, and NF-kappa B in the injured kidney. Furthermore, ACY-1215 was effective in inhibiting dedifferentiation of renal fibroblasts to myofibroblasts and the fibrotic change of renal tubular epithelial cells in culture. Collectively, these results indicate that HDAC6 inhibition can attenuate development of renal fibrosis by suppression of transforming growth factor-beta 1 and EGFR signaling and suggest that HDAC6 would be a potential therapeutic target for the treatment of renal fibrosis.