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Systems Biology of Metabolic Regulation by Estrogen Receptor Signaling in Breast Cancer
Published on: March 17, 2016
Transcriptome study of oleanolic acid in the inhibition of breast tumor growth based on high-throughput sequencing
Zhuoran Liang1,2, Ruolan Pan3, Xia Meng3
1School of Forestry, Northeast Forestry University, Harbin, Heilongjiang 150040, PR China.
Abstract:
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.
Insights
Oleanolic acid (OA) significantly inhibits breast cancer cell growth and promotes apoptosis. This study reveals OA
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Oleanolic acid (OA) has demonstrated anti-cancer properties, particularly in breast cancer.
- The precise molecular mechanisms regulating breast tumor growth under OA treatment require further investigation.
Purpose of the Study:
- To investigate the effects of OA on breast cancer cell proliferation and apoptosis in vitro and in vivo.
- To elucidate the molecular mechanisms underlying OA's anti-cancer effects using RNA sequencing.
Main Methods:
- In vitro and in vivo experiments using MCF-7 breast cancer cells and mouse models.
- RNA sequencing (RNA-seq) to analyze gene expression changes in OA-treated MCF-7 cells.
- Bioinformatic analysis of differentially expressed genes (DEGs) and pathway enrichment.
Main Results:
- OA treatment (40 μM) significantly inhibited MCF-7 cell proliferation and induced apoptosis.
- RNA-seq identified 67 downregulated and 260 upregulated DEGs in response to OA.
- Key pathways affected include p53, TNF, and mTOR signaling; specific target genes were identified.
Conclusions:
- OA exhibits a significant inhibitory effect on breast cancer growth.
- OA exerts its anti-cancer effects through modulation of specific signaling pathways and gene expression.
- Provides molecular evidence supporting OA as a potential therapeutic agent for breast cancer.

