TP53 gain-of-function mutation promotes inflammation in glioblastoma
Open accessAbstract
Glioblastoma (GBM), the most severe and common brain tumor in adults, is characterized by multiple somatic mutations and aberrant activation of inflammatory responses. Immune cell infiltration and subsequent inflammation cause tumor growth and resistance to therapy. Somatic loss-of-function mutations in the gene encoding tumor suppressor protein p53 (TP53) are frequently observed in various cancers. However, numerous studies suggest that TP53 regulates malignant phenotypes by gain-of-function (GOF) mutations. Here we demonstrate that a TP53 GOF mutation promotes inflammation in GBM. Ectopic expression of a TP53 GOF mutant induced transcriptomic changes, which resulted in enrichment of gene signatures related to inflammation and chemotaxis. Bioinformatics analyses revealed that a gene signature, upregulated by the TP53 GOF mutation, is associated with progression and shorter overall survival in GBM. We also observed significant correlations between the TP53 GOF mutation signature and inflammation in the clinical database of GBM and other cancers. The TP53 GOF mutant showed upregulated C-C motif chemokine ligand 2 (CCL2) and tumor necrosis factor alpha (TNFA) expression via nuclear factor kappa B (NFκB) signaling, consequently increasing microglia and monocyte-derived immune cell infiltration. Additionally, TP53 GOF mutation and CCL2 and TNFA expression correlated positively with tumor-associated immunity in patients with GBM. Taken together, our findings suggest that the TP53 GOF mutation plays a crucial role in inflammatory responses, thereby deteriorating prognostic outcomes in patients with GBM.
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Upregulation of CCL2 and TNFA resulted in elevated levels of microglia and monocyte-derived immune cell infiltration.
“Specifically, upregulation of CCL2 and TNFA resulted in elevated levels of microglia and monocyte-derived immune cell infiltration.”
From The p53 Pathway in Glioblastoma (2018) · cites this paper as [105]
The “TP53 R248L promotes chemotaxis” section (page unavailable) reports increased microglial and HL60-derived immune-cell migration, as well as increased microglial and macrophage infiltration in some xenografts. The “TP53 R248L upregulates CCL2 and TNFA to promote chemotaxis” section (page unavailable) shows that both cytokines increased, but the infiltration experiment identifies CCL2—not TNFA—as the mediator; CD11b+ monocyte infiltration also did not increase significantly in one tumor model. The claim therefore overstates the evidence that upregulation of both cytokines caused the reported infiltration. (LLM, conf=0.88)
Experimental — accuracy not yet measuredEnhancement of these gene signatures predicted worse prognosis and shorter survival.
“Additionally, the enhancement of these gene signatures predicted worse prognosis and shorter survival.”
From The p53 Pathway in Glioblastoma (2018) · cites this paper as [105]
The section on TP53 R248L–derived inflammatory responses reports that enrichment of TNFA signaling via NFκB negatively affected survival in patients with GBM. The section on inflammation-related transcriptomes reports shorter overall survival with TP53 R248L signature enrichment in GBM, but says that result was not statistically significant; it found no survival effect in low-grade glioma, while the combined cohort had substantially reduced survival. The unqualified claim overstates how consistently the signatures predicted shorter survival. (LLM, conf=0.86)
Experimental — accuracy not yet measuredEctopic expression of mut-p53 corresponded with enhancement of inflammatory and chemotaxis genetic signatures.
“Bioinformatic analysis revealed that the ectopic expression of mut-p53 corresponded with the enhancement of inflammatory and chemotaxis genetic signatures.”
From The p53 Pathway in Glioblastoma (2018) · cites this paper as [105]
GOF mut-p53 promotes inflammation in glioblastoma.
“Ham et al. [105] demonstrated that GOF mut-p53 promotes inflammation in GBM.”
From The p53 Pathway in Glioblastoma (2018) · cites this paper as [105]
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- Authors
- Ham, S. W., Jeon, H.-Y., Jin, X., Kim, E.-J., Kim, J.-K., Shin, Y. J., Lee, Y., Kim, S. H., Lee, S. Y., Seo, S., Park, M. G., Kim, H.-M., Nam, D.-H., & Kim, H.
- Affiliations
- Korea University (KR)
- Samsung Medical Center (KR)
- Yonsei University (KR)
- Corresponding author
- Kim, Se Hoon
- Nam, Do-Hyun
- ORCID
- Venue
- Cell Death & Differentiation
- Published
- 2018-05-21
- Volume
- 26
- Issue
- 3
- Pages
- 409-425
- ISSN
- 1350-9047 (ISSN-L)
- 1476-5403
- PMC
- PMC6370770
- OpenAlex
- W2803670454
- Cited by
- 213
- References
- 55
- Citations by year
- 2026: 10 · 2025: 26 · 2024: 31 · 2023: 25 · 2022: 35 · 2021: 38 · 2020: 34 · 2019: 12 · 2018: 2
- FWCI
- 12.16
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cell Death and Differentiation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Research Foundation (2015R1A5A1009024)
- Seoul National University
- Korea University (PJ01107701)
- Korea Health Industry Development Institute (HI14C3418)
- Seoul National University Hospital
- Samsung
- Topics
- Health Sciences › Medicine › Genetics › Glioma Diagnosis and Treatment
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Keywords
- glioblastoma, tumor inflammation, immune cell infiltration, MCP-1, TNF-α, NF-κB signaling, microglia, monocytes, prognostic gene signature, chemotaxis
- MeSH terms
- Gain of Function Mutation, Animals, Brain Neoplasms, Glioblastoma, Humans, Inflammation, Genes, p53, Tumor Suppressor Protein p53, HL-60 Cells, Cell Line, Tumor, Mice, HEK293 Cells, Heterografts
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