| 分子量(MW): | 264.3 | |
|---|---|---|
| 化学式: | C14H20N2O3 | |
| 溶解度: | DMSO ≥53mg/mL Water <1mg/mL Ethanol ≥5mg/mL | |
| 纯度: | >99% | |
| 稳定性: | at -20℃ 2 years | |
| CAS号: | 149647-78-9 |
Suberoylanilide hydroxamic acid (SAHA). Tumor suppressor genes are often silenced in human cancer; this can occur by transcriptional repression by deacetylation in the promoter regions, mediated by histone deacetylase (HDAC). HDAC inhibitors can block cancer cell growth by restoring expression of tumor suppressor genes. Vorinostat efficiently suppressed MES-SA cell growth at a low dosage (3 μM) already after 24 hours treatment. Decrease of cell survival was even more pronounced after prolonged treatment and reached 9% and 2% after 48 and 72 hours of treatment, respectively. Colony forming capability of MES-SA cells treated with 3 μM vorinostat for 24 and 48 hours was significantly diminished and blocked after 72 hours. [2]
| Vorinostat inhibits the tumor growth. NOD ⁄ SCID-B2m) ⁄ )mice were injected s.c. with 1 ・ 106 MyLa2059 cells into both flanks. When the mice had developed established palpable tumors treatment was initiated (day 1). The mice received either vehicle (black line) or 60 mg ⁄ kg vorinostat (grey line) i.p. five days a week. In total, there were four mice in the group receiving vehicle and three mice in the group receiving vorinostat. The length and width of the tumors were measured continuously until the experiment was terminated on day 20 post treatment initiation. The tumor volume was calculated using the formula V = (a ・ b2) ⁄ 2, where a defines the length (mm) and b the width (mm) of the tumor. The histogram shows the average tumor volume per flank ± SEM. * denotes a significant difference (P < 0.05) in the average tumor volume per flank between mice treated with vehicle and vorinostat at the given time-point both by using a one-tailed two samples test with Welch’s correction and a Mann–Whitney U test.
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| Vorinostat promotes C2C12 differentiation.In the image, the red is the myotube indicating differentiation ,the blue is the nuclei.
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| Western blot analysis of Acetyl-H3 and H3. 0-20μM SAHA was added.
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| SAHA induces the down-regulation of cFLIP expression and promotes TRAIL-mediated activation of a mitochondrial-operated apoptotic pathway. a BT-474 cells were treated as indicated in Fig. 1 and the cells were then harvested to analyse caspase-8, Bid, caspase-9, caspase-3 and PARP expression, using GAPDH as the protein loading control. b BT-474 cells were treated with SAHA for 8 h at the doses indicated and subsequently, the cells were harvested and the apoptosis-related proteins were analysed in western blots as described in the “Materials and Methods”. The results shown are representative of at least three independent experiments | |
| Treatment with SAHA sensitizes breast cancer cells to TRAILinduced apoptosis. BT-474 and MDA-MB-231 cells were incubated for 8 h with SAHA at the doses indicated. After this time, TRAIL (500 ng/ml) was added to some of the cultures for an additional 15 h. Apoptosis was measured as the percentage of cells with subG1 DNA content as described in the “Materials and methods”. The results show the mean and S.E.M. of three independent experiments | |
| SAHA facilitates the Itch/AIP4-independent proteasomal degradation of cFLIP proteins in breast cancer cells. a BT-474 cells were treated with SAHA (5 μM) for 8 h in the presence or absence of the proteasome inhibitors MG132 or epoxomicin (at the doses indicated), and they were then harvested and the cFLIP content was analysed in western blots. b BT-474 cells were transfected with either the siRNA oligonucleotides targeting Itch/AIP4 or the non-targeting RNA oligonucleotide (scrambled) for 48 h as described in the “Materials and Methods”. Subsequently, the cells were treated with SAHA (5 μM) for 8 h and then cFLIP and Itch/AIP4 expression was analysed in immunoblots | |
| cFLIP down-regulation following SAHA treatment is responsible for the sensitization of breast cancer cells to TRAIL. a BT-474 cells were transfected with either different siRNAs directed against the cFLIP isoforms or the non-targeting RNA oligonucleotide (scrambled) as described in the “Materials and Methods”. After 24 h, the cells were treated with TRAIL (500 ng/ml) for a further 15 h and apoptosis was then measured as the percentage of cells with subG1 DNA content. The results show the mean and S.E.M. of three independent experiments. To verify protein knockdown, cells were harvested 24 h after transfection and the cFLIP levels were assessed in immunoblots. b. BT-474 cells overexpressing Cflipl (pBABE-FLIPL) or control cells (pBABE) were treated with SAHA for 8 h at the doses indicated. After this time, TRAIL (500 ng/ml) was added to some cultures for 15 h. Apoptosis was measured as the percentage of cells with subG1 DNA content and the results show the mean and range of two independent experiments. Western blots show the cFLIP levels after SAHA treatment in pBABE and pBABE-FLIPL cells. | |
| Differential effects of HDAC inhibitors on histone and tubulin acetylation. Immunofluorescence analysis of histone H3 (K9ac/K14ac) and tubulin acetylation in HeLa cells treated for 4 h with vehicle, SAHA (10 μM), tacedinaline (50 μM), PCI-24781 (20 μM. (a) Mapping of histone acetylation in K562 cells treated with HDAC inhibitors by LC-MS/MS. Cells were treated with TSA (10 μM), SAHA (5 μM), PCI-24781 (2 μM), tacedinaline (50 μM) for 6 h. Histones were extracted from cells and acetylated peptides were quantified after isobaric tagging. |
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