ArticleHuman mutation2026
CLEC4G Promotes Pancreatic Cancer Progression by Suppressing Cathepsin B-Mediated Ferroptosis: Evidence From Mendelian Randomization Study and Experimental Validation.
Article in Human mutation, 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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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic cancer (PC) is highly lethal and lacks causal biomarkers that can inform mechanism-based therapies. Ferroptosis is an iron-dependent form of regulated cell death implicated in PC, but upstream determinants of ferroptosis in PC remain unclear. We integrated large-scale proteomic quantitative trait locus (pQTL) resources with Mendelian randomization (MR) and cell-based experiments to identify causal regulators of ferroptosis relevant to PC. Using two-sample MR with plasma pQTL data from the deCODE cohort and the UK Biobank Pharma Proteomics Project and PC genome-wide association summary statistics from FinnGen, we screened 159 FerrDb-defined ferroptosis-related proteins and identified three ferroptosis-related proteins (CTSB, IDO1, and MDM4) with significant causal effects on PC risk. A proteome-wide scan further uncovered 13 proteins associated with PC. Two-step mediation MR supported a causal pathway from CLEC4G through the ferroptosis regulator CTSB to PC risk. In vitro, CLEC4G knockdown increased CTSB expression and ferroptosis activity, which suppressed PC cell proliferation, colony formation, migration, and invasion. Together, our genetic and experimental evidence indicates that CLEC4G promotes PC progression by limiting CTSB-associated ferroptotic activity in PC cells and supports further investigation of the CLEC4G-CTSB axis in PC.
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