ArticleAmerican journal of cancer research2025
SCARA5 might be one potential marker for CC and promoted Ferroptosis by FTL.
Article in American journal of cancer research, 2025. 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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2 authors.
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Abstract
The current investigation sought to explore the effects and its possible mechanisms of Scavenger receptor class A member 5 (SCARA5) in model of colon cancer (CC). Patients diagnosed with CC were recruited from our hospital. SCARA5 mRNA expression levels in patients with CC was reduced, and the expression of SCARA5 mRNA in patients with I-II was higher than that of patients with III-IV. The overall survival (OS) and disease-free survival (DFS) of SCARA5 high expression were higher those of SCARA5 low expression in patients with CC. Sh-SCARA5 promoted CC in mice model. SCARA5 up-regulation reduced cell growth of CC. SCARA5 up-regulation promoted Ferroptosis of CC by the inhibition of mitochondrial damage. SCARA5 up-regulation induced ferritin light chain (FTL) protein expression. Si-FTL attenuated the effects of SCARA5 on Ferroptosis in CC. The SCARA5 protein interlinked with the FTL protein. SCARA5 up-regulation reduced FTL protein ubiquitination. Up-regulation of SCARA5 suppressed cell growth in CC. SCARA5 up-regulation enhanced ferroptosis in CC by inhibiting mitochondrial damage. We conclude that SCARA5 promoted ferroptosis in CC cells by inhibiting FTL ubiquitination-induced mitochondrial damage, which may contribute to the treatment of CC.
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