ArticleOncogene2009
The prolyl isomerase Pin1 regulates the NF-kappaB signaling pathway and interleukin-8 expression in glioblastoma.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- The -842G/C polymorphisms of PIN1 contributes to cancer risk: a meta-analysis of 10 case-control studies.PloS one · 2013Pooled it
- Targeting Pin1 to overcome immunosuppressive tumor microenvironment in MSS colorectal cancer.Frontiers in immunology · 2025Article
- PIN1 is a novel interaction partner and a negative upstream regulator of the transcription factor NFIB.FEBS letters · 2024Article
- Pharmacotherapeutic potential of walnut (Juglans spp.) in age-related neurological disorders.IBRO neuroscience reports · 2023Review
- Pin1 and Alzheimer's disease.Translational research : the journal of laboratory and clinical medicine · 2023Review
- Design and Synthesis of Oligopeptidic Parvulin Inhibitors.ChemMedChem · 2022Article
- Chronic Inflammation Pathway NF-κB Cooperates with Epigenetic Reprogramming to Drive the Malignant Progression of Glioblastoma.International journal of biological sciences · 2022Article
- Inhibitory effect of miR-140-5p on doxorubicin resistance of hepatocellular carcinoma.Experimental and therapeutic medicine · 2021Article
- Targeting Pin1 for Modulation of Cell Motility and Cancer Therapy.Biomedicines · 2021Review
- Anticancer Mechanism of Curcumin on Human Glioblastoma.Nutrients · 2021Review
- Natural Small Molecules Targeting NF-κB Signaling in Glioblastoma.Frontiers in pharmacology · 2021Review
- Roles of peptidyl-prolyl isomerase Pin1 in disease pathogenesis.Theranostics · 2021Review
- Xanthan gum protects temporomandibular chondrocytes from IL‑1β through Pin1/NF‑κB signaling pathway.Molecular medicine reports · 2020Article
- Deficiency of microRNA-628-5p promotes the progression of gastric cancer by upregulating PIN1.Cell death & disease · 2020Article
- Pin1 promotes pancreatic cancer progression and metastasis by activation of NF-κB-IL-18 feedback loop.Cell proliferation · 2020Article
- Pinning Down the Transcription: A Role for Peptidyl-ProlylFrontiers in cell and developmental biology · 2020Review
- Prolyl Isomerase Pin1 in Human Cancer: Function, Mechanism, and Significance.Frontiers in cell and developmental biology · 2020Review
- Function of PIN1 in Cancer Development and Its Inhibitors as Cancer Therapeutics.Frontiers in cell and developmental biology · 2020Review
- Review
- The Multiple Roles of Peptidyl Prolyl Isomerases in Brain Cancer.Biomolecules · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The brain tumor glioblastoma (GBM) remains one of the most aggressive and devastating tumors despite decades of effort to find more effective treatments. A hallmark of GBM is the constitutive activation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) signaling pathway, which regulates cell proliferation, inflammation, migration and apoptosis. The prolyl isomerase, Pin1, has been found to bind directly to the NF-kappaB protein, p65, and cause increases in NF-kappaB promoter activity in a breast cancer model. We now present evidence that this interaction occurs in GBM and that it has important consequences on NF-kappaB signaling. We demonstrate that Pin1 levels are enhanced in primary GBM tissues compared with controls, and that this difference in Pin1 expression affects the migratory capacity of GBM-derived cells. Pin1 knockdown decreases the amount of activated, phosphorylated p65 in the nucleus, resulting in inhibition of the transcriptional program of the IL-8 gene. Through the use of microarray, we also observed changes in the expression levels of other NF-kappaB regulated genes due to Pin1 knockdown. Taken together, these data suggest that Pin1 is an important regulator of NF-kappaB in GBM, and support the notion of using Pin1 as a therapeutic target in the future.
Indexed as
Identifiers
What OpenQuestion holds
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.