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Molecular & Cellular Oncology Volume 9, 2022 - Issue 1
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Commentary

Rewired lipid metabolism as an actionable vulnerability of aggressive colorectal carcinoma

Daria Capecea Department of Immunology and Inflammation, Imperial College London, London, UK;b Department of Biotechnological and Applied Clinical Sciences (DISCAB), University of L’Aquila, L’Aquila, ItalyCorrespondence[email protected]
ORCID Iconhttps://orcid.org/0000-0003-3126-2014View further author information
ORCID Icon &
Guido Franzosoa Department of Immunology and Inflammation, Imperial College London, London, UKCorrespondence[email protected]
ORCID Iconhttps://orcid.org/0000-0002-0778-988XView further author information
ORCID Icon
Article: 2024051 | Received 16 Nov 2021, Accepted 21 Dec 2021, Published online: 27 Jan 2022

Figures & data

Figure 1. Carboxylesterase (CES)1-dependent metabolic rewiring in colorectal carcinoma (CRC) etiopathogenesis. CES1 is upregulated by HNF4A and NF-κB in the Consensus Molecular Subtype (CMS)2 and CMS4 CRC subtypes and promotes tumor cell survival by increasing triacylglycerol (TAG) breakdown to fuel fatty acid oxidation (FAO) and oxidative phosphorylation (OXPHOS) during starvation and preventing toxic lipid accumulation, which triggers apoptosis and ferroptosis. as CES1 is also expressed in adipocytes, we speculate it may also play a role in the symbiosis of CRC cells with adipocytes.

Figure 1. Carboxylesterase (CES)1-dependent metabolic rewiring in colorectal carcinoma (CRC) etiopathogenesis. CES1 is upregulated by HNF4A and NF-κB in the Consensus Molecular Subtype (CMS)2 and CMS4 CRC subtypes and promotes tumor cell survival by increasing triacylglycerol (TAG) breakdown to fuel fatty acid oxidation (FAO) and oxidative phosphorylation (OXPHOS) during starvation and preventing toxic lipid accumulation, which triggers apoptosis and ferroptosis. as CES1 is also expressed in adipocytes, we speculate it may also play a role in the symbiosis of CRC cells with adipocytes.

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