ArticleCell death & disease2026
c-Myc/GRPEL1 maintains fatty acid synthesis via FASN to support PDAC cell proliferation.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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11 authors.
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Abstract
Pancreatic ductal adenocarcinoma (PDAC) cells undergo mitochondrial metabolic reprogramming to support their proliferation. However, the mechanisms by which mitochondrial protein quality control (MPQC) regulates cell metabolism remain unclear. Here, we found that c-Myc promotes PDAC cell proliferation by transcriptionally upregulating the expression of GRPEL1, an essential MPQC component. Mechanistically, c-Myc-regulated GRPEL1 maintains oxidative phosphorylation (OXPHOS) and minimizes ROS accumulation, thereby facilitating de novo fatty acid (FA) synthesis through the transcriptional upregulation of fatty acid synthase (FASN) expression. Targeting the c-Myc/GRPEL1 axis to block FASN-regulated FA synthesis inhibited PDAC cell proliferation and tumor growth in both cell models and patient-derived organoids (PDOs), whereas FA supplementation partially reversed this inhibitory effect. Clinically, c-Myc expression is positively associated with the levels of MPQC components in pancreatic ductal cells, with GRPEL1 ranking among the top hits. Furthermore, c-Myc, GRPEL1, and FASN are all expressed at higher levels in PDAC tissues than in peri-tumoral pancreatic tissues, and both c-Myc and GRPEL1 expression levels are positively correlated with that of FASN. These findings suggest that therapeutic inhibition of FA synthesis may be promising for treating PDAC patients with active c-Myc/GRPEL1/FASN signaling. Overall, this study demonstrates that FA synthesis mediated by the c-Myc/GRPEL1/FASN axis is essential for PDAC growth.
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