The function of oleanolic acid (OA) in various types of cancer has been reported frequently, especially for breast cancer. However, the regulation of breast tumor growth in response to OA treatment has not been studied in depth. Here, we first explored the effect of OA treatment on breast tumors in vitro and in vivo and then used RNA-seq technology to study the effect and molecular mechanism of OA treatment of MCF-7 cells, particularly at the level of functional genomics. The results showed that 40 μM OA treatment could significantly inhibit the proliferation and induce the apoptosis of MCF-7 cells. Through analysis of RNA sequencing data quality and differentially expressed genes (DEGs), 67 significantly downregulated genes and 260 significantly upregulated genes were identified to be involved in OA treatment of MCF-7 cells. Among these genes, 43 unique DEGs were enriched in several signaling pathways and Gene Ontology terms, such as p53 signaling pathway, TNF signaling pathway and mTOR signaling pathway. Six downregulated genes, including THBS1, EDN1, CACNG4, CCN2, AXIN2 and BMP4, as well as six upregulated genes, including ATF4, SERPINE1, SESN2, PPARGC1A, EGR1 and JAG1, were selected as target genes in response to OA treatment. The inhibitory effect of OA on breast cancer was also found in the following mouse experiments. Our study provides evidence and molecular support for the treatment of breast cancer with OA.

The aim of the present study was to perform comparative genomics using gene expression profile datasets of mice and humans who had been treated with anticancer drugs, to determine the similarities and differences in the antitumor mechanisms in the two mammals. This involved data mining of antitumor gene expression regulation, and screening of genetic loci from experimental mouse models of antitumor targets, to provide a theoretical basis of drug design. Subsequently, 9 overlapping genes with opposite expression patterns were identified across mouse and human cell lines that were treated with a specific cyclin-dependent kinase 4/6 inhibitor, PD0332991. These genes included LIM homeobox 2, adenomedullin, bone marrow stromal cell antigen 1, caveolin 1, histone cluster 1 (HIST1) H2B family member C, HIST1 H3 family member F, low density lipoprotein-receptor related protein 11, prolyl 4-hydroxylase subunit α1 and torsin family 3 member A. In addition, the janus kinase-signal transducer and activator of transcription signaling pathway, Toll-like receptor signaling pathway, T cell receptor signaling pathway and the nucleotide-binding oligomerization domain-like receptor signaling pathway were identified as candidate pathways for explaining antitumor mechanisms.

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