ArticleDiscover oncology2024
Comprehensive Mendelian randomization analysis of low-density lipoprotein cholesterol and multiple cancers.
Article in Discover oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Role of PCSK9 in breast cancer: a systematic review of its mechanistic pathways and clinical relevance.Frontiers in pharmacology · 2026Pooled it
- Cholesterol as a metabolic integrator of oncogenic signaling, immune evasion, and therapy resistance.Apoptosis : an international journal on programmed cell death · 2026Review
- Declined RTN3 stabilizes DHCR7 to induce cholesterol-dependent tumor progression and MEK inhibitors insensitivity in thyroid cancer.Cell death & disease · 2026Article
- Integrative approach to decipher pharmacological mechanism of Cinnamomum zeylanicum essential oil in prostate cancer.Medical oncology (Northwood, London, England) · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
purposeThe aim of this study was to investigate the causal relationship between low-density lipoprotein cholesterol (LDL-C) and five cancers (breast, cervical, thyroid, prostate and colorectal) using the Mendelian Randomization (MR) method, with a view to revealing the potential role of LDL-C in the development of these cancers.
methodsWe used gene variant data and disease data from the Genome-Wide Association Study (GWAS) database to assess the causal relationship between LDL-C and each cancer by Mendelian randomisation analysis methods such as inverse variance weighting and MR-Egger. Specifically, we selected Proprotein convertase subtilisin/kexin type 9 (PCSK9) and 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), genes associated with LDL-C levels, as instrumental variables, extracted the corresponding single nucleotide polymorphism (SNP) data and analysed the associations of these SNPs with five cancers.In addition, sensitivity analyses and heterogeneity tests were performed to ensure the reliability of the results.
resultsThe analyses showed that when using HMGCR gene, LDL-C were significantly and positively associated with breast (OR:1.200, 95% CI:1.082-1.329, p = 0.001), prostate (OR:1.198, 95% CI:1.050-1.366, p = 0.007), and thyroid cancers (OR:8.291, 95% CI:3.189- 21.555, p = 0.00001) were significantly positively correlated, whereas they were significantly negatively correlated with colorectal cancer (OR:0.641, 95% CI:0.442-0.928, p = 0.019); the results for cervical cancer were not significant (p = 0.050). When using the PCSK9 gene, LDL-C levels were significantly and positively associated with breast (OR:1.107, 95%:CI 1.031-1.187, p = 0.005) and prostate (OR:1.219, 95%:CI 1.101-1.349, p = 0.0001) cancers, but not with cervical (p = 0.294), thyroid cancer (p = 0.759) and colorectal cancer ( p = 0.572).
conclusionAnalyses using both the HMGCR and PCSK9 genes have shown that LDL-C may be a potential risk factor for breast and prostate cancer, while analyses of the HMGCR gene have also suggested that LDL-C may increase the risk of thyroid cancer and decrease the risk of colorectal cancer.
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