Rewired lipid metabolism as an actionable vulnerability of aggressive colorectal carcinoma.
Daria CapeceGuido FranzosoPublished in: Molecular & cellular oncology (2022)
Cancer cells reprogram lipid metabolism to fuel cell division, adaptation to stress, and metastatic dissemination. NF-κB transcription factors control this mechanism in aggressive Consensus Molecular Subtype (CMS)4 of colorectal carcinoma (CRC) via triacylglycerol (TAG) lipase, carboxylesterase 1 (CES1), thereby linking obesity-associated inflammation with metabolic adaptation and cytoprotection from lipid-induced toxicity. Our findings identify a potential therapeutic route to treat patients with metastasis-prone CRC and provide an example for targeting core tumor subtype-based vulnerabilities in cancers beyond CRC.
Keyphrases
- oxidative stress
- diabetic rats
- fatty acid
- transcription factor
- metabolic syndrome
- insulin resistance
- squamous cell carcinoma
- signaling pathway
- type diabetes
- small cell lung cancer
- single cell
- high glucose
- weight loss
- climate change
- lps induced
- weight gain
- cancer therapy
- nuclear factor
- immune response
- drug delivery
- single molecule
- stem cells
- clinical practice
- body mass index
- physical activity
- stress induced
- inflammatory response