AI Article Synopsis
- - Lipids are essential for cell membranes and play a crucial role in cell signaling and energy supply, especially when nutrients are scarce, with changes in lipid metabolism linked to cancer diversity and progression.
- - Lipid metabolism alterations are associated with epithelial-mesenchymal transition (EMT), a key process that enables tumor cells to spread, affecting various biological functions and contributing to cancer advancement.
- - Research is still needed to fully understand the mechanisms behind how lipid metabolism influences EMT, but targeting these metabolic changes may offer new ways to prevent cancer metastasis.
Article Abstract
Lipids are the key component of all membranes composed of a variety of molecules that transduce intracellular signaling and provide energy to the cells in the absence of nutrients. Alteration in lipid metabolism is a major factor for cancer heterogeneity and a newly identified cancer hallmark. Reprogramming of lipid metabolism affects the diverse cancer phenotypes, especially epithelial-mesenchymal transition (EMT). EMT activation is considered to be an essential step for tumor metastasis, which exhibits a crucial role in the biological processes including development, wound healing, and stem cell maintenance, and has been widely reported to contribute pathologically to cancer progression. Altered lipid metabolism triggers EMT and activates multiple EMT-associated oncogenic pathways. Although the role of lipid metabolism-induced EMT in tumorigenesis is an attractive field of research, there are still significant gaps in understanding the underlying mechanisms and the precise contributions of this interplay. Further study is needed to clarify the specific molecular mechanisms driving the crosstalk between lipid metabolism and EMT, as well as to determine the potential therapeutic implications. The increased dependency of tumor cells on lipid metabolism represents a novel therapeutic target, and targeting altered lipid metabolism holds promise as a strategy to suppress EMT and ultimately inhibit metastasis.
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| http://dx.doi.org/10.1007/s11010-024-04995-1 | DOI Listing |
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