ArticleOncotarget2016
The effect of epigenetic silencing and TP53 mutation on the expression of DLL4 in human cancer stem disorder.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- CHAC1 in urological tumors: contextual dualism and therapeutic implications.Frontiers in oncology · 2025Review
- The TP53-Related Signature Predicts Immune Cell Infiltration, Therapeutic Response, and Prognosis in Patients With Esophageal Carcinoma.Frontiers in genetics · 2021Article
- The α2δ1 subunit of the voltage-gated calcium channel acts as a potential candidate for breast cancer tumor initial cells biomarker.Cancer biomarkers : section A of Disease markers · 2021Article
- DNA Methylation Activates TP73 Expression in Hepatocellular Carcinoma and Gastrointestinal Cancer.Scientific reports · 2019Article
- Role of Jagged1/STAT3 signalling in platinum-resistant ovarian cancer.Journal of cellular and molecular medicine · 2019Article
- Functional roles of CTCF in breast cancer.BMB reports · 2017Article
- Breast cancer in patients with Li-Fraumeni syndrome - a case-series study and review of literature.Breast cancer (Dove Medical Press) · 2017Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The Li-Fraumeni Syndrome (LFS), a genetically rare heterogeneous cancer syndrome, is characterized primarily by a germline p53 (TP53) gene mutation. We recently discovered a balanced reciprocal chromosomal translocation t(11;15)(q23;q15) in the non-cancerous skin fibroblasts of a bilateral breast cancer patient in LFS family. This prompted us to investigate the breakpoint region of the translocation, which uncovered a gene that encodes a Notch ligand, DLL4, (locus at 15q15.1), a key target in tumor vasculature. We analyzed DLL4 gene expression and protein level in LFS non-cancerous skin fibroblast cell lines and non-LFS cancer cell lines. DLL4 is abrogated in all the LFS cells and drastically down-regulated in breast (MCF7) and brain (IMR32) cancer cells and tumor tissue samples. However, DNA methylation studies revealed that DLL4 promoter is silenced only in MCF7 but not in LFS cells. We further investigated the regulation of DLL4 gene expression by ChIP assays, which demonstrated that p53 binds to DLL4 promoter through its association with CTCF, a chromosomal networking protein CCCTC binding factor. This implies a possible karyotype-phenotype correlation with respect to DLL4 in LFS and breast cancer initiation and progression. The drastic reduction or absence in the expression of DLL4 in LFS as well as breast and brain cancer cells is significant and supports the concept that this ligand may also play a role in cancer immune-surveillance; and its resuscitation in the tumor microenvironment may stimulate T-cell immunity and suppress tumor growth. Therefore, DLL4 may provide a strong platform as an immuno-therapeutic target in LFS and cancer patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.