ArticleJournal of experimental & clinical cancer research : CR2023
Integrated multi-dimensional analysis highlights DHCR7 mutations involving in cholesterol biosynthesis and contributing therapy of gastric cancer.
Article in Journal of experimental & clinical cancer research : CR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- A novel pathogenic synonymous DHCR7 variant unveiled by aberrant splicing in Smith-Lemli-Opitz syndrome.Human genetics · 2026Article
- Multitrait GWAS and functional validation reveal genetic loci for gastric cancer.Nature communications · 2026Article
- Declined RTN3 stabilizes DHCR7 to induce cholesterol-dependent tumor progression and MEK inhibitors insensitivity in thyroid cancer.Cell death & disease · 2026Article
- DHCR7 Promotes Liver Metastasis of Pancreatic Cancer Through PI3K-Akt Signaling Pathway.Cancer science · 2025Article
- DHCR7 as a Prognostic and Immunological Biomarker in Human Pan-Cancer: A Comprehensive Evaluation.Cancer reports (Hoboken, N.J.) · 2025Article
- Targeting lipid metabolism: novel insights and therapeutic advances in pancreatic cancer treatment.Lipids in health and disease · 2025Review
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- 7-Dehydrocholesterol Reductase Activates the Hedgehog Pathway by Regulating Cholesterol to Promote the Development of Triple-Negative Breast Cancer.Current cancer drug targets · 2025Article
- Effect ofAnimal biotechnology · 2024Article
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- TMEM147 aggravates the progression of HCC by modulating cholesterol homeostasis, suppressing ferroptosis, and promoting the M2 polarization of tumor-associated macrophages.Journal of experimental & clinical cancer research : CR · 2023Article
- Investigating the Diagnostic and Therapeutic Potential of SREBF2-Related Lipid Metabolism Genes in Colon Cancer.OncoTargets and therapy · 2023Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundGenetic background plays an important role in the occurrence and development of gastric cancer (GC). With the application of genome-wide association study (GWAS), an increasing number of tumor susceptibility genes in gastric cancer have been discovered. While little of them can be further applicated in clinical diagnosis and treatment due to the lack of in-depth analysis.
methodsA GWAS of peripheral blood leukocytes from GC patients was performed to identify and obtain genetic background data. In combination with a clinical investigation, key SNP mutations and mutated genes were screened. Via in vitro and in vivo experiments, the function of the mutated gene was verified in GC. Via a combination of molecular function studies and amino acid network analysis, co-mutations were discovered and further identified as potential therapeutic targets.
resultsAt the genetic level, the G allele of rs104886038 in DHCR7 was a protective factor identified by the GWAS. Clinical investigation showed that patients with the rs104886038 A/G genotype, age ≥ 60, smoking ≥ 10 cigarettes/day, heavy drinking and H. pylori infection were independent risk factors for GC, with odds ratios of 12.33 (95% CI, 2.10 ~ 72.54), 20.42 (95% CI, 2.46 ~ 169.83), and 11.39 (95% CI, 1.82 ~ 71.21), respectively. Then molecular function studies indicated that DHCR7 regulated cell proliferation, migration, and invasion as well as apoptosis resistance via cellular cholesterol biosynthesis pathway. Further amino acid network analysis based on the predicted structure of DHCR7 and experimental verification indicated that rs104886035 and rs104886038 co-mutation reduced the stability of DHCR7 and induced its degradation. DHCR7 mutation suppressed the malignant behaviour of GC cells and induced apoptosis via inhibition on cell cholesterol biosynthesis.
conclusionIn this work, we provided a comprehensive multi-dimensional analysis strategy which can be applied to in-depth exploration of GWAS data. DHCR7 and its mutation sites identified by this strategy are potential theratic targets of GC via inhibition of cholesterol biosynthesis.
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