Trichothecin
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| Category | Antibiotics |
| Catalog number | BBF-02713 |
| CAS | 6379-69-7 |
| Molecular Weight | 332.39 |
| Molecular Formula | C19H24O5 |
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Description
Trichothecin has anti-fungal and protozoal effects and it's produced by the strain of Trichothecium roseum.
Specification
| Synonyms | NSC 92492; 12,13-Epoxy-4-hydroxytrichothec-9-en-8-one crotonate |
| IUPAC Name | [(1S,2R,7R,9R,11R,12S)-1,2,5-trimethyl-4-oxospiro[8-oxatricyclo[7.2.1.02,7]dodec-5-ene-12,2'-oxirane]-11-yl] (Z)-but-2-enoate |
| Canonical SMILES | CC=CC(=O)OC1CC2C3(C1(C4(CC(=O)C(=CC4O2)C)C)C)CO3 |
| InChI | InChI=1S/C19H24O5/c1-5-6-16(21)24-14-8-15-19(10-22-19)18(14,4)17(3)9-12(20)11(2)7-13(17)23-15/h5-7,13-15H,8-10H2,1-4H3/b6-5-/t13-,14-,15-,17+,18-,19+/m1/s1 |
| InChI Key | LJWZOKOFCBPNAG-HULHSAFCSA-N |
| Source | Trichothecenes are produced on many different grains like wheat, oats or maize by various Fusarium species such as F. graminearum, F. sporotrichioides, F. poae and F. equiseti. |
Properties
| Appearance | Colorless Acicular Crystal |
| Antibiotic Activity Spectrum | fungi |
| Boiling Point | 451.179°C at 760 mmHg |
| Melting Point | 117°C |
| Density | 1.241 g/cm3 |
Toxicity
| Carcinogenicity | No indication of carcinogenicity to humans (not listed by IARC). |
| Mechanism Of Toxicity | Trichothecin is a trichothecene mycototoxin. Unlike many other mycotoxins, trichothecenes do not require metabolic activation to exert their biological activity, instead directly reacting with cellular components. Trichothecenes are cytotoxic to most eukaryotic cells due to their powerful ability to inhibit protein synthesis. They do this by freely moving across the plasma membrane and binding specifically to ribosomes with high-affinity. Specifically, they interfere with the active site of peptidyl transferase at the 3'-end of large 28S ribosomal RNA and inhibit the initiation, elongation or termination step of protein synthesis, as well as cause polyribosomal disaggregation. Protein synthesis is an essential function in all tissues, but tissues where cells are actively and rapidly growing and dividing are very susceptible to the toxins. Additionally, binding to ribosomes is thought to activate proteins in downstream signalling events related to immune response and apoptosis, such as mitogen-activated protein kinases. This is known as ribotoxic stress response. Trichothecenes may also induce some alterations in membrane structure, leading to increased lipid peroxidation and inhibition of electron transport activity in the mitochondria. They can further induce apoptosis through generation of reactive oxygen species. Further secondary effects of trichothecenes include inhibition of RNA and DNA synthesis, and also inhibition of mitosis. |
Reference Reading
1. Trichothecin inhibits invasion and metastasis of colon carcinoma associating with SCD-1-mediated metabolite alteration
Chaoliang Liao, Min Li, Xiang Li, Namei Li, Xu Zhao, Xiaoyi Wang, Yawen Song, Jing Quan, Can Cheng, Jikai Liu, Ann M Bode, Ya Cao, Xiangjian Luo Biochim Biophys Acta Mol Cell Biol Lipids. 2020 Feb;1865(2):158540. doi: 10.1016/j.bbalip.2019.158540. Epub 2019 Oct 31.
Lipid metabolic abnormalities have received intensified concerns and increased de novo synthesis of lipids is recognized as a common feature of many human cancers. Nevertheless, the role of lipid metabolism that confers aggressive properties on human cancers still remains to be revealed. Natural compounds represent an abundant pool of agents for the discovery of novel lead compounds. Trichothecin (TCN) is a sesquiterpenoid originating from an endophytic fungus of the herbal plant Maytenus hookeri Loes. Here, we assess the association of stearoyl-CoA desaturase 1 (SCD-1) over-expression with malignant progression of colorectal cancer (CRC). Based on this association, the effect of TCN on migration and invasion of colon carcinoma cells closely related to the inhibition of SCD-1 is evaluated. We further demonstrate that reduced production of unsaturated fatty acids (FAs) by blocking SCD-1 activity is beneficial for the anti-invasion effect of TCN. The aim of this study was to clarify the mechanistic connection between metabolite alterations induced by metabolic rewiring and the aggressive tumor phenotype and further develop novel pharmacological tools for the intervention of tumor invasion associated with SCD-1-mediated metabolite alterations.
2. Trichothecin Inhibits Cancer-Related Features in Colorectal Cancer Development by Targeting STAT3
Xin Qi, Meng Li, Xiao-Min Zhang, Xiu-Fen Dai, Jian Cui, De-Hai Li, Qian-Qun Gu, Zhi-Hua Lv, Jing Li Molecules. 2020 May 14;25(10):2306. doi: 10.3390/molecules25102306.
Signal transducer and activator of transcription 3 (STAT3) is a transcription factor that contributes to cancer progression through multiple processes of cancer development, which makes it an attractive target for cancer therapy. The IL-6/STAT3 pathway is associated with an advanced stage in colorectal cancer patients. In this study, we identified trichothecin (TCN) as a novel STAT3 inhibitor. TCN was found to bind to the SH2 domain of STAT3 and inhibit STAT3 activation and dimerization, thereby blocking STAT3 nuclear translocation and transcriptional activity. TCN did not affect phosphorylation levels of STAT1. TCN significantly inhibited cell growth, arrested cell cycle at the G0/G1 phase, and induced apoptosis in HCT 116 cells. In addition, the capacities of colony formation, migration, and invasion of HCT 116 cells were impaired upon exposure to TCN with or without IL-6 stimulation. In addition, TCN treatment abolished the tube formation of HUVEC cells in vitro. Taken together, these results highlight that TCN inhibits various cancer-related features in colorectal cancer development in vitro by targeting STAT3, indicating that TCN is a promising STAT3 inhibitor that deserves further exploration in the future.
3. DHRS2 mediates cell growth inhibition induced by Trichothecin in nasopharyngeal carcinoma
Xiangjian Luo, Namei Li, Xu Zhao, Chaoliang Liao, Runxin Ye, Can Cheng, Zhijie Xu, Jing Quan, Jikai Liu, Ya Cao J Exp Clin Cancer Res. 2019 Jul 10;38(1):300. doi: 10.1186/s13046-019-1301-1.
Background: Cancer is fundamentally a deregulation of cell growth and proliferation. Cancer cells often have perturbed metabolism that leads to the alteration of metabolic intermediates. Dehydrogenase/reductase member 2 (DHRS2) belongs to short-chain alcohol dehydrogenase/reductase (SDR) superfamily, which is functionally involved in a number of intermediary metabolic processes and in the metabolism of lipid signaling molecules. DHRS2 displays closely association with the inhibition of cell proliferation, migration and quiescence in cancers. Methods: 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4- sulfophenyl)-2H-tetrazolium (MTS), 5-ethynyl-2'-deoxyuridine (EdU) and colony formation assays were applied to evaluate the proliferative ability of nasopharyngeal carcinoma (NPC) cells. We performed lipid metabolite profiling using gas chromatography coupled with mass spectrometry (GC/MS) to identify the proximal metabolite changes linked to DHRS2 overexpression. RNA sequencing technique combined with differentially expressed genes analysis was applied to identify the expression of genes responsible for the anti-tumor effect of trichothecin (TCN), a natural sesquiterpenoid compound isolated from an endophytic fungus. Results: Our current findings reveal that DHRS2 affects lipid metabolite profiling to induce cell cycle arrest and growth inhibition in NPC cells. Furthermore, we demonstrate that TCN is able to induce growth inhibition of NPC in vitro and in vivo by up-regulating DHRS2. Conclusions: Our report suggests that activating DHRS2 to reprogram lipid homeostasis may be a target for the development of targeted therapies against NPC. Moreover, TCN could be exploited for therapeutic gain against NPC by targeting DHRS2 and it may also be developed as a tool to enhance understanding the biological function of DHRS2.
Spectrum
Predicted LC-MS/MS Spectrum - 10V, Positive
Experimental Conditions
Ionization Mode: Positive
Collision Energy: 10 eV
Instrument Type: QTOF (generic), spectrum predicted by CFM-ID
Mass Resolution: 0.0001 Da
Collision Energy: 10 eV
Instrument Type: QTOF (generic), spectrum predicted by CFM-ID
Mass Resolution: 0.0001 Da
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Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
