ArticleOncotarget2015
Function of phosphorylation of NF-kB p65 ser536 in prostate cancer oncogenesis.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 83 citations in OpenAlex.
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- Effect of regulatory cell death on the occurrence and development of head and neck squamous cell carcinoma.Biomarker research · 2023Review
- Drivers of Radioresistance in Prostate Cancer.Journal of clinical medicine · 2022Review
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- Biological relevance of ZNF224 expression in chronic lymphocytic leukemia and its implication IN NF-kB pathway regulation.Frontiers in molecular biosciences · 2022Article
- MEX3D is an oncogenic driver in prostate cancer.The Prostate · 2021Article
- MEST promotes lung cancer invasion and metastasis by interacting with VCP to activate NF-κB signaling.Journal of experimental & clinical cancer research : CR · 2021Article
- Roles of long noncoding RNAs on tumor immune escape by regulating immune cells differentiation and function.American journal of cancer research · 2021Review
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- Multiplexing information flow through dynamic signalling systems.PLoS computational biology · 2020Article
- Nitidine chloride inhibits the appearance of cancer stem-like properties and regulates potential the mitochondrial membrane alterations of colon cancer cells.Annals of translational medicine · 2020Article
- Exportin 1 Inhibition Induces Nerve Growth Factor Receptor Expression to Inhibit the NF-κB Pathway in Preclinical Models of Pediatric High-Grade Glioma.Molecular cancer therapeutics · 2020Article
- MiR-1307-5p targeting TRAF3 upregulates the MAPK/NF-κB pathway and promotes lung adenocarcinoma proliferation.Cancer cell international · 2020Article
- Cardamonin attenuates chronic inflammation and tumorigenesis in colon.Cell cycle (Georgetown, Tex.) · 2019Article
- The interaction of YBX1 with G3BP1 promotes renal cell carcinoma cell metastasis via YBX1/G3BP1-SPP1- NF-κB signaling axis.Journal of experimental & clinical cancer research : CR · 2019Article
- Clusterin Silencing in Prostate Cancer Induces Matrix Metalloproteinases by an NF-Journal of oncology · 2019Article
- Absence of GdX/UBL4A Protects against Inflammatory Diseases by Regulating NF-кB Signaling in Macrophages and Dendritic Cells.Theranostics · 2019Article
- Lymphotoxin α fine-tunes T cell clonal deletion by regulating thymic entry of antigen-presenting cells.Nature communications · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Majority of prostate cancer (PCa) patients carry TMPRSS2/ERG (T/E) fusion genes and there has been tremendous interest in understanding how the T/E fusion may promote progression of PCa. We showed that T/E fusion can activate NF-kB pathway by increasing phosphorylation of NF-kB p65 Ser536 (p536), but the function of p536 has never been studied in PCa. We report here that active p536 can significantly increase cell motility and transform PNT1a cells (an immortalized normal cell line), suggesting p536 plays a critical role in promoting PCa tumorigenesis. We have discovered a set of p536 regulated genes, among which we validated the regulation of CCL2 by p536. Based on all evidence, we favor that T/E fusion, NF-kB p536 and CCL2 form a signaling chain. Finally, PNT1a cells (not tumorigenic) can form tumors in SCID mice when overexpressing of either wild type or active p65 in the presence of activated AKT, demonstrating synergistic activities of NF-kB and AKT signals in promoting PCa tumorigenesis. These findings indicate that combination therapies targeting T/E fusion, NF-kB, CCL2 and/or AKT pathways may have efficacy in T/E fusion gene expressing PCa. If successful, such targeted therapy will benefit more than half of PCa patients who carry T/E fusions.
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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 Socratic graph.