Trichostatin A (TSA),58880-19-6,IC-0219614

Trichostatin A (TSA) is A potent histone deacetylase (HDAC) inhibitor and an antifungal antibiotic with an IC50 value of 1.8 nM for HDAC[1], which has the properties of inhibiting cell growth and inducing cell differentiation.
Trichostatin A (TSA) can arrest cells in G1 and G2 phases, induce cell differentiation, and restore transformed morphology of cultured cells. Trichostatin A (TSA) inhibits proliferation of breast cancer cells in human breast cancer cell linesand resulted in hyperacetylation of histone H4[1]. Trichostatin A (TSA) promotes apoptosis and radiation-induced DNA damage in mitotic G2 gap 2 (G2/M) -arrested cells. Trichostatin A (TSA) may directly participate in DNA damage in esophageal cancer cells by reducing the acetylation of growth-associated genomic protein H3[2].Pre-treatment of RLE-6TN cells with Trichostatin A (TSA) inhibited radiation-induced EMT-like morphological alterations including elevated protein level of α-SMA and Snail, reduction of E-cadherin expression, enhanced phosphorylation of GSK3β and ERK1/2, increased generation of ROS[3].The invasive and migratory abilities of MCF-7 cells were suppressed significantly upon treatment with Trichostatin A (TSA). Treatment with Trichostatin A (TSA) led to an increased expression level of E-cadherin, and decreased expression of vimentin and, in MCF-7 cells[4]. Trichostatin A (TSA) enhanced the radiosensitivity of colon cancer cells, apoptotic cell death induced by radiation was enhanced by Trichostatin A (TSA) treatment. Trichostatin A (TSA) also induced autophagic response in colon cancer cells, while autophagy inhibition led to cell apoptosis and enhanced the radiosensitivity of colon cancer cells[5].
Trichostatin A (TSA) had pronounced antitumor activity in vivo when administered to 16 animals at a dose of 500 microg/kg by injection daily for 4 weeks compared with 14 control animals. Furthermore, Trichostatin A (TSA) did not cause any measurable toxicity in doses of up to 5 mg/kg by injection. Trichostatin A (TSA) has significant antitumor activity in vivo The antitumor activity of Trichostatin A (TSA) is attributed to differentiation induction[1].In porcine SCNT embryos,Chaetocin, Trichostatin A (TSA), and the combination significantly increased the cleavage and blastocyst formation rate, hatching/hatched blastocyst rate, and cell numbers and survival rate. The combined treatment improved the rate of development to blastocysts more so than chaetocin or Trichostatin A (TSA) alone[6].This decreased emotionality observed in stress-maladaptive mice was significantly recovered by chronic treatment with Trichostatin A (TSA) 2 h before daily exposure to restraint stress, which confirmed the development of stress adaptation. HDAC inhibitor Trichostatin A (TSA) may have a beneficial effect on stress adaptation by affecting 5-HT neural function in the brain and alleviate the emotional abnormality under conditions of excessive stress[7].