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SLC6A8-mediated creatine uptake suppresses ERK2-FSP1 signaling and induces ferroptosis in colorectal cancer

ABSTRACT: To explore whether creatine regulates iron death sensitivity in colorectal cancer by modulating the function of certain proteins, we performed immunoprecipitation experiments with biotin-labelled creatine and conducted proteomics studies on these IP-down proteins.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Colon Cancer

SUBMITTER: zhou xiaojun

LAB HEAD: Li Youjun

PROVIDER: PXD061637 | Pride | 2025-09-06

REPOSITORIES: Pride

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Publications

SLC6A8-mediated creatine uptake suppresses ERK2-FSP1 signaling and induces ferroptosis in colorectal cancer.

Zhou Xiaojun X Wang Genxin G Wu Yuhang Y Wu Mingzhi M Zhai Xiang X Tian Chenhui C Prochownik Edward V EV Jiang Congqing C Li Youjun Y

Cell reports 20250901 9

Tumor metabolic reprogramming is critical for providing energy to support proliferation and resistance to stress-induced cell death. However, the regulatory mechanisms linking these processes remain incompletely understood. Here, using untargeted metabolomics, we demonstrate that creatine potently induces ferroptosis in colorectal cancer (CRC). Mechanistically, creatine binds extracellular signal-regulated kinase 2 (ERK2), impairing its activation by mitogen-activated protein kinase kinase 1 (ME ...[more]

PMID: 40892544

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SLC6A8-mediated creatine uptake suppresses ERK2-FSP1 signaling and induces ferroptosis in colorectal cancer

Project description:We discovered, through untargeted metabolomics, that creatine promotes ferroptosis in colorectal cancer. Our study identifies ERK2 as a creatine sensor that mediates active FSP1 and ferroptosis resistance, and highlights the potential of targeting tumor SLC6A8 for cancer treatment.

2025-09-05 | GSE285466 | GEO

SLC6A8-mediated creatine uptake suppresses ERK2-FSP1 signaling and induces ferroptosis in colorectal cancer

Project description:SLC6A8-mediated creatine uptake suppresses ERK2-FSP1 signaling and induces ferroptosis in colorectal cancer

| PRJNA1203678 | ENA

Metabolic reprogramming of macrophage polarization by creatine [ATAC-seq]

Project description:We found that the creatine metabolic pathway was differentially regulated under M1 versus M2 polarizing conditions. In return, creatine could suppress M1 by blocking STAT1 tyrosine phosphorylation while promote M2 by sustaining chromatin accessibility of specific gene loci.

2019-08-06 | GSE110403 | GEO

Metabolic reprogramming of macrophage polarization by creatine [RNA-seq]

2019-08-06 | GSE110395 | GEO

Effect of acute creatine monohydrate supplementation on skeletal muscle transcriptome

Project description:Expression profiling of vastus lateralis muscle of young, healthy, non-obese men supplemented with creatine monohydrate vs. placebo for 10 days. Results identify transcriptional pathways activated in skeletal muscles as a result of acute creatine monohydrate supplementation. Keywords: Supplementation response. In a randomized, placebo-controlled, crossover, double-blind design, 12 young, healthy, non-obese men were supplemented with either a placebo or creatine monohydrate (loading phase, 20 g/d x 3 d; maintenance phase, 5 g/d x 7 d) for 10 d. Following a 28 day washout period, subjects were put on the alternate supplementation for 10 days. Muscle biopsies of the vastus lateralis were obtained and were assessed for global mRNA expression using cDNA microarrays.

2010-06-11 | E-GEOD-7877 | biostudies-arrayexpress

Defective DcpS Decapping Manifests in Creatine Deficiency Syndrome and Neurological impairment

Project description:Biallelic mutations in the DCPS gene that disrupt the decapping activity of the DcpS scavenger decapping enzyme lead to neurodevelopmental deficiencies and intellectual disability. However, how the neurogenesis defects arise in these individuals remains unknown. Here we show that cells derived from DCPS mutant individuals have a metabolic deficiency in their creatine biosynthetic pathway. The cells possess reduced levels of creatine and a corresponding elevation of the creatine precursor, guanidinoacetate (GAA), due to reduced levels of guanidinoacetate methyltransferase mRNA and protein. Importantly, the compromised neurogenesis as well as neurite outgrowth observed in DcpS mutant induced pluripotent stem cell differentiation into neurons was reversed upon supplementation of creatine monohydrate into the culture medium. These findings suggest creatine deficiency as the underlying etiology of the neurogenetic defect in DcpS mutant cells and a potential driver of the neurological deficienciesin affected individuals.

2025-05-30 | GSE274722 | GEO

Effect of acute creatine monohydrate supplementation on skeletal muscle transcriptome

2007-05-23 | GSE7877 | GEO

Creatine increases health and life span in mice

Project description:Here we show that oral creatine (Cr) supplementation leads to increased life span in mice. Treated mice showed improved neurobehavioral performance, decreased accumulation of the aging pigment lipofuscin and upregulation of “anti-aging” genes in brain. As Cr is virtually free of adverse effects, it may be a promising food supplement for healthy aging in man. Keywords: creatine, life span, neurobehavioural performance, microarray, oxidative stress, aging

2007-06-13 | GSE5140 | GEO

Transcription profiling of brains from mice fed with or without creatine supplementation to study the molecular mechanism of creatine improving health and life span in mice

Project description:Here we show that oral creatine (Cr) supplementation leads to increased life span in mice. Treated mice showed improved neurobehavioral performance, decreased accumulation of the aging pigment lipofuscin and upregulation of anti-aging genes in brain. As Cr is virtually free of adverse effects, it may be a promising food supplement for healthy aging in man. Experiment Overall Design: 6 biological replicates for creatine-treated mice, 7 biological replicates for untreated mice.

2007-11-22 | E-GEOD-5140 | biostudies-arrayexpress

Increased phosphocreatine/creatine ratio in white adipocytes promotes inflammation

Project description:The mechanisms promoting disturbed white adipocyte function in obesity remain largely unclear. Herein, we integrate white adipose tissue (WAT) metabolomic and transcriptomic data from clinical cohorts and find that the WAT phosphocreatine/creatine ratio is increased and creatine kinase-B expression and activity is decreased in the obese state. . In human in vitro and murine in vivo models, we demonstrate that decreased phosphocreatine metabolism in white adipocytes alters AMPK activity via effects on ATP/ADP levels, independently of WAT beigeing. This disturbance promotes a pro-inflammatory profile characterized, in part, by increased CCL2 production. These data suggest that the phosphocreatine/creatine system links cellular energy shuttling with pro-inflammatory responses in human and murine white adipocytes. Our findings provide unexpected perspectives on the mechanisms driving WAT inflammation in obesity and may present avenues to target adipocyte dysfunction.

2022-01-27 | GSE192361 | GEO