Related Experiment Video
Updated: Aug 2, 2026
09:19
Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo
Published on: February 6, 2015
8.7K
Integrated Metabolomics and Transcriptomics Analysis of Anacardic Acid Inhibition of Breast Cancer Cell Viability
Kellianne M Piell1, Claire C Poulton1, Christian G Stanley1
1Department of Biochemistry & Molecular Genetics, University of Louisville School of Medicine, Louisville, KY 40292, USA.
International Journal of Molecular Sciences
|July 13, 2024
Summary
Anacardic acid (AnAc) effectively inhibits breast cancer (BC) cell growth by disrupting lipid biosynthesis and increasing cellular stress. This study reveals AnAc
Area of Science:
- Molecular Biology
- Cancer Research
- Metabolomics
Background:
- Estrogen receptor α (ERα)-positive and triple-negative breast cancer (TNBC) exhibit distinct metabolic vulnerabilities.
- Anacardic acid (AnAc) shows potential as an anti-cancer agent, but its precise mechanisms in breast cancer remain incompletely understood.
- Understanding AnAc's impact on cellular metabolism is crucial for developing targeted breast cancer therapies.
Purpose of the Study:
- To investigate the impact of Anacardic acid (AnAc) on the cellular metabolism of breast cancer (BC) cells.
- To identify key metabolic pathways and molecular signaling affected by AnAc treatment in ERα-positive and triple-negative BC (TNBC) cell lines.
- To explore the metabolic diversity among different TNBC subtypes in response to AnAc.
Main Methods:
- RNA sequencing (seq) and network analysis of AnAc-treated MCF-7 and MDA-MB-231 breast cancer (BC) cells.
- Comprehensive untargeted metabolomics analysis of control versus AnAc-treated MCF-7, MDA-MB-231, MDA-MB-468, BT-20, and HCC1806 cells.
- Integration of transcriptomic and metabolomic data to identify signaling pathways regulated by AnAc.
Main Results:
- Anacardic acid (AnAc) inhibited lipid biosynthesis and increased endoplasmic reticulum stress in both ERα-positive and triple-negative breast cancer (TNBC) cells.
- Metabolomic analysis revealed significant metabolic alterations in AnAc-treated cells, affecting pathways including alanine, aspartate, glutamate, glutathione, pentose phosphate, and citric acid cycle.
- Integration of transcriptomic and metabolomic data identified mTORC1 downstream signaling as a key pathway affected by AnAc in both cell lines.
Conclusions:
- Anacardic acid (AnAc) differentially alters cellular building blocks, nutrients, and transcripts in breast cancer (BC) cells, leading to reduced cell viability.
- AnAc exhibits anti-proliferative effects on both ERα-positive and triple-negative breast cancer (TNBC) cells by targeting key metabolic pathways.
- The findings highlight AnAc's potential as a therapeutic agent for breast cancer, with implications for understanding TNBC heterogeneity.
