Anisomycin, an antibiotic isolated from Streptomyces griseus, is also a JNK activator. Anisomycin inhibited protein synthesis mainly by inhibiting ribosomal subunit peptidyl transferase activity at 80S. Additionally, anisomycin induces apoptosis in various cell types through the activation of the P38, JNK, and ERK1/2 pathways, making it a promising chemotherapeutic drug for cancer[1-4].
Anisomycin(10-100nM; 24h) reduces cell viability in a concentration-dependent manner in B16 melanoma cells[5]. Anisomycin(1-80 ng/ml; 24h) may activate the P53/P21/P27 signaling pathway to reduce the expression of ICBP90, inhibit the expression of P-CDK2 to block cells in the S and G2/M phases, and ultimately lead to the inhibition of Jurkat T cell proliferation [6]. Anisomycin(31.8 μM) inhibits the proliferation, migration, and angiogenesis of OCSCs by altering the expression of antisense RNA NCBP2-AS2[7].
Anisomycin(5 mg/kg; i.p; 3 weeks) effectively disrupts breast cancer angiogenesis by impairing capillary network formation, inhibiting cell migration, proliferation, and survival in MD-MBA-231 cell-based breast cancer models[8]. Anisomycin(2-200μg/kg; i.p; 30days) upregulates utrophin protein levels in mdx mouse diaphragm[9].
References：
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[2]. Hall SS, Loebenberg D, et,al. Structure-activity relationships of synthetic antibiotic analogues of anisomycin. J Med Chem. 1983 Apr;26(4):469-75. doi: 10.1021/jm00358a003. PMID: 6834379.
[3]. Schmeits PC, Katika MR, et,al. DON shares a similar mode of action as the ribotoxic stress inducer anisomycin while TBTO shares ER stress patterns with the ER stress inducer thapsigargin based on comparative gene expression profiling in Jurkat T cells. Toxicol Lett. 2014 Jan 30;224(3):395-406. doi: 10.1016/j.toxlet.2013.11.005. Epub 2013 Nov 15. PMID: 24247028.
[4]. Slipicevic A, Øy GF, et,al. Low-dose anisomycin sensitizes melanoma cells to TRAIL induced apoptosis. Cancer Biol Ther. 2013 Feb;14(2):146-54. doi: 10.4161/cbt.22953. Epub 2012 Nov 28. PMID: 23192275; PMCID: PMC3571996.
[5]. Ushijima H, Monzaki R, et,al. Suppressive Effects of Anisomycin on the Proliferation of B16 Mouse Melanoma Cells In Vitro. Anticancer Res. 2021 Dec;41(12):6113-6121. doi: 10.21873/anticanres.15431. PMID: 34848466.
[6]. Yu C, Xing F, et,al. Anisomycin suppresses Jurkat T cell growth by the cell cycle-regulating proteins. Pharmacol Rep. 2013;65(2):435-44. doi: 10.1016/s1734-1140(13)71019-3. PMID: 23744428.
[7]. Ling L, Wen Y, et,al. Anisomycin inhibits the activity of human ovarian cancer stem cells via regulating antisense RNA NCBP2-AS2/MEK/ERK/STAT3 signaling. J Gene Med. 2024 Jan;26(1):e3571. doi: 10.1002/jgm.3571. Epub 2023 Jul 22. PMID: 37483091.
[8]. Yang W, Zhou C, et,al. Anisomycin inhibits angiogenesis, growth, and survival of triple-negative breast cancer through mitochondrial dysfunction, AMPK activation, and mTOR inhibition. Can J Physiol Pharmacol. 2022 Jul 1;100(7):612-620. doi: 10.1139/cjpp-2021-0577. Epub 2022 Jul 19. PMID: 35852219.
[9]. Hadwen J, Farooq F, et,al. Anisomycin Activates Utrophin Upregulation Through a p38 Signaling Pathway. Clin Transl Sci. 2018 Sep;11(5):506-512. doi: 10.1111/cts.12562. Epub 2018 Jun 7. PMID: 29877606; PMCID: PMC6132359.
Anisomycin是一种从灰链霉菌中分离出来的抗生素，也是一种JNK激活剂。Anisomycin主要通过抑制80S核糖体亚基肽基转移酶活性来抑制蛋白质合成。Anisomycin可通过激活P38、JNK和ERK1/2通路诱导多种细胞类型的凋亡，是一种很有前景的癌症化疗药物[1-4]。
Anisomycin(10-100nM; 24h)以浓度依赖性的方式降低B16黑色素瘤细胞的细胞活力[5]。Anisomycin(1-80 ng/ml; 24h)可激活P53/P21/P27信号通路，降低ICBP90的表达，抑制P-CDK2的表达，使细胞进入S期和G2/M期，最终抑制Jurkat T细胞的增殖[6]。Anisomycin(31.8 μM)可以通过调节反义RNA NCBP2-AS2的表达抑制OCSCs的增殖、迁移和血管生成[7]。
Anisomycin(5 mg/kg; i.p; 3 weeks)通过抑制乳腺癌小鼠MD-MBA-231细胞毛细血管网络的形成、迁移、增殖和存活，有效靶向乳腺癌血管生成[8] 。Anisomycin(2-200μg/kg;i.p; 30days)上调MDX小鼠膈肌肌营养蛋白水平[9]。