Research Paper Volume 13, Issue 19 pp 22883—22897
Transcriptome study of oleanolic acid in the inhibition of breast tumor growth based on high-throughput sequencing
- 1 School of Forestry, Northeast Forestry University, Harbin, Heilongjiang 150040, PR China
- 2 Harbin Vocational and Technical College, Harbin, Heilongjiang 150081, PR China
- 3 Center for Stem Cell and Translational Medicine, School of Life Sciences, Anhui University, Hefei, Anhui 230601, PR China
Received: May 15, 2021 Accepted: September 18, 2021 Published: October 4, 2021https://doi.org/10.18632/aging.203582
How to Cite
Copyright: © 2021 Liang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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.