ArticleScientific reports2019
Synergistic activation of the NEU4 promoter by p73 and AP2 in colon cancer cells.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Sialylation of cell surface glycoconjugates modulates cytosolic galectin-mediated responses upon organelle damage : Minireview.Glycoconjugate journal · 2023Review
- P63 and P73 Activation in Cancers with p53 Mutation.Biomedicines · 2022Review
- Transcriptomics and transmission ultrastructural examination reveals the nephrotoxicity of cadmium in laying hens.Environmental science and pollution research international · 2022Article
- NAMPT Inhibitor and P73 Activator Represses P53 R175H Mutated HNSCC Cell Proliferation in a Synergistic Manner.Biomolecules · 2022Article
- Fragile GeneFrontiers in oncology · 2021Article
- Heparan Sulfate Facilitates Spike Protein-Mediated SARS-CoV-2 Host Cell Invasion and Contributes to Increased Infection of SARS-CoV-2 G614 Mutant and in Lung Cancer.Frontiers in molecular biosciences · 2021Article
- Roles of p53 Family Structure and Function in Non-Canonical Response Element Binding and Activation.International journal of molecular sciences · 2019Review
- GEPIA2: an enhanced web server for large-scale expression profiling and interactive analysis.Nucleic acids research · 2019Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
More than 50% of colon cancers bear mutations in p53, one of the most important tumor suppressors, and its family members p63 or p73 are expected to contribute to inhibiting the progression of colon cancers. The AP2 family also acts as a tumor suppressor. Here we found that p73 and AP2 are able to activate NEU4, a neuraminidase gene, which removes the terminal sialic acid residues from cancer-associated glycans. Under serum starvation, NEU4 was up-regulated and one of the NEU4 target glycans, sialyl Lewis X, was decreased, whereas p73 and AP2 were up-regulated. Sialyl Lewis X levels were not, however, decreased under starvation conditions in p73- or AP2-knockdown cells. p53 and AP2 underwent protein-protein interactions, exerting synergistic effects to activate p21, and interaction of p53 with AP2 was lost in cells expressing the L350P mutation of p53. The homologous residues in p63 and p73 are L423 and L377, respectively. The synergistic effect of p53/p63 with AP2 to activate genes was lost with the L350P/L423P mutation in p53/p63, but p73 bearing the L377P mutation was able to interact with AP2 and exerted its normal synergistic effects. We propose that p73 and AP2 synergistically activate the NEU4 promoter in colon cancer cells.
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