Abstract |
The association between intratumoral cholesteryl ester (CE) and tumor progression has been reported previously. The objective of our study was to investigate a causal effect of CE on mammary tumor progression. Using MMTV-PyMT (MMTV-polyoma virus middle T) transgenic mice and breast tumor cell MCF-7, we show that both exogenous and endogenous CE can increase mammary tumor growth, that CE upregulates the AKT/mTOR pathway, and that CE synthesis blockade suppresses this signaling pathway. Our data suggest that SOAT1, a sterol O-acyltransferase, may be a potential target for the treatment of breast cancer.
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Authors | Lengyun Wei, Xuyang Lu, Shengmei Weng, Shenglong Zhu, Yongquan Chen |
Journal | Biomolecules
(Biomolecules)
Vol. 11
Issue 6
(06 08 2021)
ISSN: 2218-273X [Electronic] Switzerland |
PMID | 34201030
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Cholesterol Esters
- Sterol O-Acyltransferase
- sterol O-acyltransferase 1
- mTOR protein, mouse
- Proto-Oncogene Proteins c-akt
- TOR Serine-Threonine Kinases
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Topics |
- Animals
- Cholesterol Esters
(genetics, metabolism)
- Female
- Humans
- MCF-7 Cells
- Mammary Neoplasms, Animal
(drug therapy, genetics, metabolism, pathology)
- Mice
- Mice, Transgenic
- Proto-Oncogene Proteins c-akt
(genetics, metabolism)
- Signal Transduction
- Sterol O-Acyltransferase
(genetics, metabolism)
- TOR Serine-Threonine Kinases
(genetics, metabolism)
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