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Eduardo, M. B.

Publications and source records attributed to Eduardo, M. B..

2 recordsLinked to original sources

Medium-Chain Fatty Acid exposure in non-transformed mammary glands leads to pro-tumorigenic alterations associated with aging

The local breast environment is a valuable research focus for identifying the etiological and biological factors that contribute to the development of breast cancer. Single-cell RNA sequencing shows that the increased availability of the medium-chain fatty acid octanoic acid induces changes typical of the aged mammary gland, including downregulation of cell-cell junctions, altered extracellular matrix (ECM)-receptor interactions, and upregulation of aging markers like MDK and GDF15. Ex vivo exposure to medium-chain fatty acids compromises cell-cell junctions leading to cell dissemination. As aging is associated with an increased risk of developing breast cancer, it is crucial to identify the factors driving these age-related changes in the mammary gland to develop effective cancer prevention strategies. Given that the proportion of breast adipocytes increases with age, we propose that the remodeling of the mammary gland associated with aging is partly due to the increase in adipocytes and fatty-acid release.

cancer biology↗

Metabolic shift to serine pathway induced by lipids confers oncogenic properties in non-transformed breast cells

A lipid metabolism gene signature is associated with the risk of estrogen negative breast cancer (ER-BC). In vitro, lipid exposure alters histone methylation affecting gene expression and increasing flux through various metabolic reactions; but little is known about the mechanism(s) linking lipids and epigenetic reprogramming with the genesis of ER-BC. Here we show that the metabolism of the medium-chain fatty acid Octanoic Acid (OA) in preference to glucose and glutamine results in a metabolic shift toward the serine pathway increasing the production of SAM, glutathione, and 2-HG, with implications for oncogenesis: SAM production results in epigenetic fostered plasticity leading to reprogramming/selecting cells that express Neural, EMT and BC related genes. 2-HG exposure results in appearance of DNA breaks, potentially consequent to the inhibition of essential demethylases for HR repair. ROS increases shortly after OA exposure and is mitigated by antioxidant defenses, which favors/enables the survival of specific cell subtypes.

cancer biology↗