ArticleHuman genomics2024
Growth characteristics of HCT116 xenografts lacking asparagine synthetase vary according to sex.
Article in Human genomics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Article
- CXCL5 neutralization mitigates cancer cachexia by disrupting CAF-cancer cell crosstalk.Journal of biomedical science · 2025Article
- Exploring the anticancer potential of nitrated N-substituted-4-hydroxy-2-quinolone-3-carboxamides: synthesis, biological assessment, and computational analysis.BMC chemistry · 2025Article
- Sex-specific effects of exogenous asparagine on colorectal tumor growth, 17β-estradiol levels, and aromatase.Pharmacological research · 2025Article
- Targeting Asparagine Metabolism in Solid Tumors.Nutrients · 2025Review
- Role of sex steroids in colorectal cancer: pathomechanisms and medical applications.American journal of cancer research · 2024Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundSex-related differences in colorectal (CRC) incidence and mortality are well-documented. However, the impact of sex on metabolic pathways that drive cancer growth is not well understood. High expression of asparagine synthetase (ASNS) is associated with inferior survival for female CRC patients only. Here, we used a CRISPR/Cas9 technology to generate HCT116 ASNS
resultsASNS loss reduces cancer burden in male and female tumor-bearing mice (40% reduction, q < 0.05), triggers metabolic reprogramming including gluconeogenesis, but confers a survival improvement (30 days median survival, q < 0.05) in female tumor-bearing mice alone. Transcriptomic analyses revealed upregulation of G-protein coupled estrogen receptor (GPER1) in tumors from male and female mice with HCT116 ASNS
conclusionsOur study indicates that inferior survival for female CRC patients with high ASNS may be due to metabolic reprogramming that sustains tumor growth. These findings have translational relevance as ASNS/GPER1 signaling could be a future therapeutic target to improve the survival of female CRC patients.
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Registered trials
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