ArticleFrontiers in pharmacology2024
Upregulation of GOLPH3 mediated by Bisphenol a promotes colorectal cancer proliferation and migration: evidence based on integrated analysis.
Article in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Multi-scale evidence chain: Linking environmental BPA exposure to ovarian cancer through integrated omics and experimental models.Translational oncology · 2026Article
- GOLPH3 promotes papillary thyroid carcinoma by regulating the TGF-β signaling pathway.Molecular genetics and genomics : MGG · 2026Article
- Assessing the role of ultra-processed foods in colorectal cancer incidence: insights from the EPIC cohort.BMC public health · 2026Article
- Identifying Metabolic Signatures of Bisphenol Analog Exposure: Implication for Rapid Toxicity Screening of New Alternatives.Environmental science & technology · 2025Article
- Protective Effect of Melatonin Against Bisphenol A Toxicity.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
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Abstract
Background: The interaction between environmental endocrine-disrupting chemicals, such as Bisphenol A (BPA), and their influence on cancer progression, particularly regarding the GOLPH3 gene in colorectal cancer, remains unclear. Methods: We performed an integrated analysis of transcriptional profiling, clinical data, and bioinformatics analyses utilizing data from the Comparative Toxicogenomics Database and The Cancer Genome Atlas. The study employed ClueGO, Gene Set Enrichment Analysis, and Gene Set Variation Analysis for functional enrichment analysis, alongside experimental assays to examine the effects of BPA exposure on colorectal cancer cell lines, focusing on GOLPH3 expression and its implications for cancer progression. Results: Our findings demonstrated that BPA exposure significantly promoted the progression of colorectal cancer by upregulating GOLPH3, which in turn enhanced the malignant phenotype of colorectal cancer cells. Comparative analysis revealed elevated GOLPH3 protein levels in cancerous tissues Conclusion: This study provides novel insights into the complex interactions between BPA exposure and GOLPH3 in the context of colorectal cancer, emphasizing the need for heightened awareness and measures to mitigate BPA exposure risks. Our findings advocate for further research to validate these observations in clinical and epidemiological settings and explore potential therapeutic targets within these pathways.
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