Chaetocin

Manufactured by Enzo Life Sciences

Sourced in United States

Chaetocin is a fungal metabolite that functions as a histone methyltransferase inhibitor. It can inhibit the activity of the histone-lysine N-methyltransferase enzyme SUV39H1.

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Lab products found in correlation

4 protocols using chaetocin

Epigenetic Modifiers in Cell Treatment

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After passaging, cells were treated for 24 h with 1 µM GSK343 (Ezh2 inhibitor, Sigma-Aldrich), 100 nM 5-Aza (DNA methylation inhibitor, Sigma-Aldrich), 100 nM chaetocin (Suv39h1 inhibitor, Enzo-LifeScience) or 100 nM Hesperadin (Aurkb inhibitor, Sigma-Aldrich), from stock solutions prepared in DMSO.

Djeghloul D., Dimond A., Cheriyamkunnel S., Kramer H., Patel B., Brown K., Montoya A., Whilding C., Wang Y.F., Futschik M.E., Veland N., Montavon T., Jenuwein T., Merkenschlager M, & Fisher A.G. (2023). Loss of H3K9 trimethylation alters chromosome compaction and transcription factor retention during mitosis. Nature Structural & Molecular Biology, 30(4), 489-501.

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Cell Culture and Compound Screening

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HepG2, Hep3B and Huh7 cells were cultured in DMEM medium containing 10% fetal bovine serum (Hyclone, Waltham, MA, USA), penicillin and streptomycin. Chaetocin was purchased from Enzo Life Sciences (Farmingdale, NY, USA). The pan-caspase inhibitor z-VAD-fmk was purchased from R&D Systems (Minneapolis, MN, USA). Baf.A1 was purchased from LC Laboratories (Woburn, MA, USA). Rapamycin was purchased from Calbiochem (La Jolla, CA, USA).

Jung H.J., Seo I., Casciello F., Jacquelin S., Lane S.W., Suh S.I., Suh M.H., Lee J.S, & Baek W.K. (2016). The anticancer effect of chaetocin is enhanced by inhibition of autophagy. Cell Death & Disease, 7(2), e2098-.

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Oxidative Stress and Epigenetic Modulators

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Deferoxamine (DFO), CoCl₂, 2-methoxyestradiol (2-ME), N-acetyl-L-cysteine (NAC), MitoTEMPO, U0126, 5-aza-2’-deoxycytidine (5-aza-dC), Y294002, SB203580, Ro31-8220, rapamycin, BML-275, trichostatin A (TSA) and 2’,7’-dichlorofluorescein diacetate (DCF-DA) were obtained from Sigma-Aldrich (St Louis, MO. USA), and MitoPQ, MitoSOX-Red and 2‐(N‐(7‐nitrobenz‐2‐oxa‐1,3‐diazol‐4‐yl)amino)‐2‐deoxyglucose (2‐NBD‐glucose) were from Abcam (Cambridge, UK), Thermo Fisher Scientific (Waltham, MA, USA) and Life Technologies (Carlsbad, CA, USA), respectively. AR-C155858 and SP600125 were supplied by Tocris Bioscience (Bristol, UK), and, syrosingopine was obtained from Extrasynthese SA (Lyon, France), respectively. TX-402 was a gift from Dr. H. Nagasawa, Gifu Pharmaceutical University. rapamycin was purchased from LC Laboratories (Woburn, MA, USA); BAY11-7082 was from AdipoGen Life Sciences (San Diego, CA, USA); PF-4708671 and KU-0063794 were from Selleck Chemicals LLC (Houston, TX, USA), and chaetocin was from Enzo Life Science (Farmingdale, NY, USA).

Takenaga K., Koshikawa N., Akimoto M., Tatsumi Y., Lin J., Itami M, & Nagase H. (2021). MCT4 is induced by metastasis-enhancing pathogenic mitochondrial NADH dehydrogenase gene mutations and can be a therapeutic target. Scientific Reports, 11, 13302.

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Investigating Small-Molecule Modulators in HCC Cell Lines

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Human HCC cell lines Huh7, Hep3B, MH97H and PDK4-MH97H cells with stable PDK4 overexpression were maintained in DMEM (Gibco, NY) with 10% fetal bovine serum (Gibco) and 100 U/ml penicillin-streptomycin (Mediatech, VA) (15 (link)–17 (link)). PDK4-MH97H cells were generated by retroviral gene transfer with recombinant MSCV expression vectors (pMSCVPDK4). Isolation and culturing of primary hepatocytes were described previously (18 (link), 19 (link)). For small-molecule inhibitor treatment, Huh7, Hep3B and MH97H cells were treated with vehicle control (DMSO), 2 and 10 µM of BRD4770 (Sigma, MO) or 0.1 and 0.5 µM of Chaetocin (Enzo Life Sciences, NY) for 48 h. For arsenic exposure, Huh7, Hep3B and PDK4-MH97H cells were cultured in growth medium containing various concentrations of NaAsO₂ (Sigma) (0.1-50 µM) for 3 ~ 24 h. For a combination treatment, cells were cultured in medium containing DMSO control (Ctrl group), 24h 1.0 µM NaAsO₂ (As group), 48h 10 µM BRD4770 (BRD group) and 10 µM BRD4770 plus 1.0 µM NaAsO₂ (BRD + As group). G9a siRNA (sc-43777) was purchased from Santa Cruz.

Zhang X., Wu J., Choiniere J., Yang Z., Huang Y., Bennett J, & Wang L. (2016). Arsenic silences hepatic PDK4 expression through activation of histone H3K9 methylatransferase G9a. Toxicology and applied pharmacology, 304, 42-47.

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