Mammary tumor growth and pulmonary metastasis are enhanced in a hyperlipidemic mouse model
Open accessAbstract
Dyslipidemia has been associated with an increased risk for developing cancer. However, the implicated mechanisms are largely unknown. To explore the role of dyslipidemia in breast cancer growth and metastasis, we used the apolipoprotein E (ApoE) knockout mice (ApoE(-/-)), which exhibit marked dyslipidemia, with elevated circulating cholesterol and triglyceride levels in the setting of normal glucose homeostasis and insulin sensitivity. Non-metastatic Met-1 and metastatic Mvt-1 mammary cancer cells derived from MMTV-PyVmT/FVB-N transgenic mice and c-Myc/vegf tumor explants respectively, were injected into the mammary fat pad of ApoE(-/-) and wild-type (WT) females consuming a high-fat/high-cholesterol diet and tumor growth was evaluated. ApoE(-/-) mice exhibited increased tumor growth and displayed a greater number of spontaneous metastases to the lungs. Furthermore, intravenous injection of Mvt-1 cells resulted in a greater number of pulmonary metastases in the lungs of ApoE(-/-) mice compared with WT controls. To unravel the molecular mechanism involved in enhanced tumor growth in ApoE(-/-) mice, we studied the response of Mvt-1 cells to cholesterol in vitro. We found that cholesterol increased Akt(S473) phosphorylation in Mvt-1 cells as well as cellular proliferation, whereas cholesterol depletion in the cell membrane abrogated Akt(S473) phosphorylation induced by exogenously added cholesterol. Furthermore, in vivo administration of BKM120, a small-molecule inhibitor of phosphatidylinositol 3-kinase (PI3K), alleviated dyslipidemia-induced tumor growth and metastasis in Mvt-1 model with a concomitant decrease in PI3K/Akt signaling. Collectively, we suggest that the hypercholesterolemic milieu in the ApoE(-/-) mice is a favorable setting for mammary tumor growth and metastasis.
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Tumors grown in hypercholesterolemic mice (ApoE−/−) have increased PI3K and AKT signaling, and treatment with a PI3K inhibitor attenuated growth.
“One example of this comes from tumors grown in hypercholesterolemic mice (ApoE−/−), which have increased PI3K and AKT signaling, and treatment with a PI3K inhibitor was able to attenuate growth (78).”
From Cholesterol efflux protein, ABCA1, supports anticancer functions of myeloid immune cells (2026) · cites this paper as [78]
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Self-citation
- Authors
- Alikhani, N., Ferguson, R. D., Novosyadlyy, R., Gallagher, E. J., Scheinman, E. J., Yakar, S., & LeRoith, D.
- Affiliations
- Mount Sinai Hospital (US)
- Rambam Health Care Campus (IL)
- Corresponding author
- LeRoith, D
- Venue
- Oncogene
- Published
- 2012-04-02
- Volume
- 32
- Issue
- 8
- Pages
- 961-967
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- PMC
- PMC4063440
- OpenAlex
- W1982833706
- Cited by
- 146
- References
- 41
- Citations by year
- 2026: 6 · 2025: 10 · 2024: 6 · 2023: 10 · 2022: 11 · 2021: 11 · 2020: 13 · 2019: 11 · 2018: 7 · 2017: 12 · 2016: 17 · 2015: 10 · 2014: 8 · 2013: 13 · 2012: 1
- FWCI
- 3.40
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Israel Cancer Association
- National Cancer Institute (R01CA128799)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Keywords
- dyslipidemia, hypercholesterolemia, breast cancer, mammary tumor growth, lung metastasis, ApoE-deficient mice, cholesterol, Akt phosphorylation, PI3K/Akt signaling, BKM120, high-fat high-cholesterol diet, c-Myc, vascular endothelial growth factor, tumor cell proliferation
- MeSH terms
- Animals, Disease Models, Animal, Female, Humans, Hypercholesterolemia, Lung Neoplasms, Mammary Neoplasms, Experimental, Mice, Transgenic, Neoplasm Metastasis, Signal Transduction, Cell Line, Tumor, Cell Growth Processes, Mice
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