Page last updated: 2024-10-15

chaetocin

Description

chaetocin: inhibits G9a histone methyltransferase [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

Cross-References

ID SourceID
PubMed CID146158463
MeSH IDM0043141

Synonyms (2)

Synonym
chaetocin
28097-03-2

Research Excerpts

Overview

Chaetocin is a widely used chemical that decreases H3K9 methylation in cells. It has a potent anti-proliferative pharmacological activity on various cancer cells. Chaetomium species fungi belong to the thiodiketopyrazines.

ExcerptReference
"Chaetocin is a natural metabolite product with various biological activities and pharmacological functions isolated from Chaetomium species fungi belonging to the thiodiketopyrazines. "( Chaetocin: A review of its anticancer potentials and mechanisms.
Jiang, H; Li, L; Li, Y; Liu, K; Su, Q; Tang, Z; Xiang, X; Zhang, X, 2021
)
"Chaetocin is a widely used chemical that decreases H3K9 methylation in cells."( Chaetocin disrupts the SUV39H1-HP1 interaction independent of SUV39H1 methyltransferase activity.
Han, L; Indermaur, EW; Keung, AJ; Lee, JB, 2023
)
"Chaetocin is a small-molecule natural product produced by Chaetomium species fungi, and it has a potent anti-proliferative pharmacological activity on various cancer cells. "( Chaetocin induces apoptosis in human melanoma cells through the generation of reactive oxygen species and the intrinsic mitochondrial pathway, and exerts its anti-tumor activity in vivo.
Han, X; Han, Y; Ma, T; Sun, Q; Xu, L; Zhang, J; Zheng, Y, 2017
)
"Chaetocin is a fungal metabolite that possesses a potential anti-inflammatory activity. "( Chaetocin attenuates gout in mice through inhibiting HIF-1α and NLRP3 inflammasome-dependent IL-1β secretion in macrophages.
Chen, H; Chen, S; Liu, F; Lu, J; Ma, Y; Zhang, M, 2019
)
"Chaetocin is a compound isolated from fungal cultures and has been reported as a potent and selective inhibitor of suppressor of variegation 3-9 homolog 1 (Suv39h1), which catalyzes histone methylation on histone H3 lysine 9 (H3K9) residues."( Chaetocin inhibits RANKL-induced osteoclast differentiation through reduction of Blimp1 in Raw264.7 cells.
Imai, K; Murofushi, T; Ochiai, K; Suzuki, N; Tsuda, H; Yang, P; Zhao, N, 2015
)
"Chaetocin is a natural product isolated from Chaetomium species that has anti-bacterial and anti-myeloma activities. "( Chaetocin inhibits IBMX-induced melanogenesis in B16F10 mouse melanoma cells through activation of ERK.
Bae, JS; Chung, JH; Han, M; Yao, C, 2016
)
"Chaetocin is a fungal metabolite that possesses a potent antiproliferative activity in solid tumors by inducing cell death. "( The anticancer effect of chaetocin is enhanced by inhibition of autophagy.
Baek, WK; Casciello, F; Jacquelin, S; Jung, HJ; Lane, SW; Lee, JS; Seo, I; Suh, MH; Suh, SI, 2016
)
"Chaetocin is a thiodioxopiperazine produced by fungi belonging to the chaetomiaceae family."( Effect of chaetocin on renal cell carcinoma cells and cytokine-induced killer cells.
Rombo, R; Schmidt-Wolf, IG; Weiher, H, 2016
)

Actions

ExcerptReference
"Chaetocin did not suppress the H3K9me3 modification in porcine embryonic fibroblast (PEF) but downregulated the expression of suv39h1, suv39h2, and kdm4d."( Improvement in the in vitro development of cloned pig embryos after kdm4a overexpression and an H3K9me3 methyltransferase inhibitor treatment.
Cai, MM; Liu, C; Liu, Y; Liu, ZH; Weng, XG; Zhang, YT, 2020
)

Treatment

Chaetocin treatment upregulates reactive oxygen species (ROS) production as well as the transcription of death-receptor-related genes, in a ROS-dependent manner. Co-treatment with chaetOCin and HDAC inhibitor trichostatin A (TSA) dramatically increased apoptosis.

ExcerptReference
"Chaetocin-treated tumors exhibited heightened ROS, pATM, YAP1 and pJNK levels."( Chaetocin-induced ROS-mediated apoptosis involves ATM-YAP1 axis and JNK-dependent inhibition of glucose metabolism.
Anto, NP; Dixit, D; Ghildiyal, R; Sen, E, 2014
)
"Chaetocin treatment activated endoplasmic reticulum (ER) stress which gave rise to the up-regulation of ATF3 and CHOP."( Chaetocin induces endoplasmic reticulum stress response and leads to death receptor 5-dependent apoptosis in human non-small cell lung cancer cells.
Guo, S; Liu, X; Su, L, 2015
)
"Chaetocin treatment upregulates reactive oxygen species (ROS) production as well as the transcription of death-receptor-related genes, in a ROS-dependent manner, leading to death receptor-dependent apoptosis."( Anti-leukemia activity of chaetocin via death receptor-dependent apoptosis and dual modulation of the histone methyl-transferase SUV39H1.
Altucci, L; Castellano, R; Chaib, H; Collette, Y; Garbit, S; Nebbioso, A; Prebet, T; Restouin, A; Vey, N, 2012
)
"Treatment with chaetocin increased the radiation sensitivity of cells in vitro and DNA damage response, especially of 53BP1 and ATM-dependent repair by affecting chromatin structure. "( Chaetocin induced chromatin condensation: effect on DNA repair signaling and survival.
Bannik, K; Groneberg, M; Sak, A; Stuschke, M, 2021
)
"Co-treatment with chaetocin and HDAC inhibitor trichostatin A (TSA) dramatically increased apoptosis and produced greater activation of genes."( Improved therapeutic effect against leukemia by a combination of the histone methyltransferase inhibitor chaetocin and the histone deacetylase inhibitor trichostatin A.
Ahn, JS; Kim, HJ; Kim, HN; Kim, YK; Kook, H; Lee, IK; Lee, JJ; Nguyen-Pham, TN; Park, KS; Tran, HT, 2013
)
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (69)

TimeframeStudies, This Drug (%)All Drugs %
pre-19901 (1.45)18.7374
1990's0 (0.00)18.2507
2000's3 (4.35)29.6817
2010's56 (81.16)24.3611
2020's9 (13.04)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials0 (0.00%)5.53%
Reviews5 (7.14%)6.00%
Case Studies0 (0.00%)4.05%
Observational0 (0.00%)0.25%
Other65 (92.86%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]