ArticleEnvironmental science and pollution research international2022
Bioinformatics analysis of key genes and potential mechanism in cadmium-induced breast cancer progression.
Article in Environmental science and pollution research international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 6 citations in OpenAlex.
- NUPR1 in breast cancer: mechanisms and potential applications.Frontiers in physiology · 2026Review
- A label-free microLC-SWATH-MS methodology with immunoaffinity depletion of highly abundant serum proteins for quantitative proteomic comparison of fresh-frozen human normal breast tissue and tumor clinical specimens.Frontiers in molecular biosciences · 2026Article
- Article
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8 authors at 2 institutions in 1 country.
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Abstract
Cadmium (Cd) may be associated with breast cancer progression, but the detailed molecular mechanism has not been fully elucidated. In this study, one public dataset (GSE136595) was used to identify differentially expressed genes (DEGs) in Cd-treated MCF-7 breast cancer cells. We determined a total of 2077 DEGs, and Ingenuity Pathway Analysis (IPA) software showed that 246 of them were related to tumor progression. Pathway analysis of these DEGs indicated that the HIF1α signaling and the epithelial-mesenchymal transition (EMT) pathway regulated by growth factors might be activated. Moreover, twist family bHLH transcription factor 1 (TWIST1), lysine demethylase 3A (KDM3A), Kruppel-like factor 4 (KLF4), nuclear protein 1 (NUPR1), neurogenin 3 (NEUROG3), and HNF1 homeobox B (HNF1B) might be the key transcription factors. And the result of protein-protein interaction (PPI) analysis showed that the hub genes in these 246 DEGs were tumor protein p53 (TP53), polo-like kinase 1 (PLK1), sirtuin 1 (SIRT1), protein tyrosine phosphatase non-receptor type 11 (PTPN11), caspase 8 (CASP8), cyclin-dependent kinase 6 (CDK6), calmodulin 3 (CALM3), KRAS proto-oncogene (KRAS), extra spindle pole bodies like 1 (ESPL1), and marker of proliferation Ki-67 (MKI67). Further analysis indicated that TWIST1, NUPR1, KRAS, and PTPN11 were related to the prognostic of breast cancer based on the Cancer Genome Atlas (TCGA) and they were validated to be upregulated in the Cd-treated MCF-7 cells. Our results suggested that the HIF1α signaling and the EMT pathway regulated by growth factors might be participant in the Cd-induced breast cancer progression and TWIST1, NUPR1, KRAS, and PTPN11 might be potential key genes.
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