Anisomycin is used as a chemical compound that possesses c-Jun N-terminal kinase (JNK)-activating effects. Recently, the potent anti-tumor effects of anisomycin have received much attention. In addition to its JNK-activating effects, anisomycin has been reported to affect gene expression in osteosarcoma, leukemia, hepatocellular carcinoma, ovarian cancer and other cancers. We previously demonstrated that anisomycin induced the degradation of transcription factor GATA-6 in DLD-1 cells (a colorectal cancer cell line) and inhibited their proliferation. However, the details of the gene network involved in the process remain unclear. In this study, we conducted an RNA-seq analysis of differentially expressed genes (DEGs) in anisomycin-treated DLD-1 cells to identify the molecular process of growth-suppressive genes. We found that LAMB3, which regulates cell adhesion and migration, and NFKB2 were down-regulated by anisomycin. In addition, the mRNA expression of several tumor suppressor genes (ATF3, ERRFI1, KLF6, and AKAP12) was transiently enhanced at 3 h after anisomycin treatment. These results suggest that anisomycin blocks a PI3K/Akt-signaling cascade to lead to the suppression of cell growth.
Keywords: ATF3; Anisomycin; CPM, counts per million; DLD-1; DLD-1, a colorectal adenocarcinoma cell line isolated by D. L. Dexter and associates; DMSO, dimethyl sulfoxide; FBS, fetal bovine serum; GO, gene ontology; JNK, c-Jun N-terminal kinase; KEGG, Kyoto Encyclopedia of Genes and Genomes; LAMB3; PBS, phosphate buffered saline; RNA-seq; RNA-seq, RNA sequencing.
© 2021 The Authors. Published by Elsevier B.V.