Metabolic profiling of triple-negative breast cancer cells reveals metabolic vulnerabilities
Open accessAbstract
BACKGROUND: Among breast cancers, the triple-negative breast cancer (TNBC) subtype has the worst prognosis with no approved targeted therapies and only standard chemotherapy as the backbone of systemic therapy. Unique metabolic changes in cancer progression provide innovative therapeutic opportunities. The receptor tyrosine kinases (RTKs) epidermal growth factor receptor (EGFR), and MET receptor are highly expressed in TNBC, making both promising therapeutic targets. RTK signaling profoundly alters cellular metabolism by increasing glucose consumption and subsequently diverting glucose carbon sources into metabolic pathways necessary to support the tumorigenesis. Therefore, detailed metabolic profiles of TNBC subtypes and their response to tyrosine kinase inhibitors may identify therapeutic sensitivities. METHODS: We quantified the metabolic profiles of TNBC cell lines representing multiple TNBC subtypes using gas chromatography mass spectrometry. In addition, we subjected MDA-MB-231, MDA-MB-468, Hs578T, and HCC70 cell lines to metabolic flux analysis of basal and maximal glycolytic and mitochondrial oxidative rates. Metabolic pool size and flux measurements were performed in the presence and absence of the MET inhibitor, INC280/capmatinib, and the EGFR inhibitor, erlotinib. Further, the sensitivities of these cells to modulators of core metabolic pathways were determined. In addition, we annotated a rate-limiting metabolic enzymes library and performed a siRNA screen in combination with MET or EGFR inhibitors to validate synergistic effects. RESULTS: TNBC cell line models displayed significant metabolic heterogeneity with respect to basal and maximal metabolic rates and responses to RTK and metabolic pathway inhibitors. Comprehensive systems biology analysis of metabolic perturbations, combined siRNA and tyrosine kinase inhibitor screens identified a core set of TCA cycle and fatty acid pathways whose perturbation sensitizes TNBC cells to small molecule targeting of receptor tyrosine kinases. CONCLUSIONS: Similar to the genomic heterogeneity observed in TNBC, our results reveal metabolic heterogeneity among TNBC subtypes and demonstrate that understanding metabolic profiles and drug responses may prove valuable in targeting TNBC subtypes and identifying therapeutic susceptibilities in TNBC patients. Perturbation of metabolic pathways sensitizes TNBC to inhibition of receptor tyrosine kinases. Such metabolic vulnerabilities offer promise for effective therapeutic targeting for TNBC patients.
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Modulation of cancer-specific metabolic adaptations weakens malignant cells and widens the therapeutic window for effective treatment of TNBC patients.
“The modulation of cancer-specific metabolic adaptations weakens the malignant cells and widens the therapeutic window for effective treatment of TNBC patients (Lanning et al., 2017; Wang et al., 2020).”
From An Arthropod Hormone, Ecdysterone, Inhibits the Growth of Breast Cancer Cells via Different Mechanisms (2020) · cites this paper as Lanning et al., 2017
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“In contrast, ER+ breast cancer cells have been found to be more dependent on OXPHOS, even when glycolysis is functioning (Rodriguez-Enriquez et al., 2010; Lanning et al., 2017).”
BackgroundShuvalov, O., Fedorova, O., Tananykina, E., Gnennaya, Y., Daks, A., Petukhov, A., & Barlev, N. A. (2020) · Frontiers in Pharmacology · doi:10.3389/fphar.2020.561537 · Cited by 30 · see citing works
- Authors
- Lanning, N. J., Castle, J. P., Singh, S. J., Leon, A. N., Tovar, E. A., Sanghera, A., MacKeigan, J. P., Filipp, F. V., & Graveel, C. R.
- Affiliations
- California State University Los Angeles (US)
- Van Andel Institute (US)
- University of California, Merced (US)
- Corresponding author
- Lanning, Nathan J.
- Graveel, Carrie R.
- ORCID
- Venue
- Cancer & Metabolism
- Published
- 2017-08-22
- Volume
- 5
- Issue
- 1
- Pages
- 6-6
- ISSN
- 2049-3002 (ISSN-L)
- PMC
- PMC5568171
- OpenAlex
- W2748503909
- Cited by
- 175
- References
- 76
- Citations by year
- 2026: 15 · 2025: 15 · 2024: 17 · 2023: 18 · 2022: 23 · 2021: 26 · 2020: 29 · 2019: 17 · 2018: 14 · 2017: 1
- FWCI
- 5.60
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Cancer & Metabolism (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Cancer Institute (CA159709, CA154887)
- Breast Cancer Research Foundation (N/A)
- University of California Cancer Research Coordinating Committee research grant (N/A)
- Health Science Research Institute Grant (N/A)
- The Frederik and Lena Meijer Student Internship Program (N/A)
- The Van Andel Foundation (N/A)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Keywords
- triple-negative breast cancer, metabolite profiling, receptor tyrosine kinase, EGFR, MET, capmatinib, erlotinib, tyrosine kinase inhibitors, metabolic heterogeneity, glycolysis, mitochondrial respiration, TCA cycle, fatty acid metabolism, siRNA screen, drug synergy, metabolic vulnerability
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