ArticleNagoya journal of medical science2009
Mutated ras induced PLD1 gene expression through increased Sp1 transcription factor.
Article in Nagoya journal of medical science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed, 11 citations in OpenAlex.
- PLD1 is a key player in cancer stemness and chemoresistance: Therapeutic targeting of cross-talk between the PI3K/Akt and Wnt/β-catenin pathways.Experimental & molecular medicine · 2024Review
- BPDE, the Migration and Invasion of Human Trophoblast Cells, and Occurrence of Miscarriage in Humans: Roles of a NovelEnvironmental health perspectives · 2023Article
- Tissue microarray staining reveals PLD1 and Sp1 have a collaborative, pro-tumoral effect in patients with osteosarcomas.Oncotarget · 2017Article
- Functional regulation of phospholipase D expression in cancer and inflammation.The Journal of biological chemistry · 2014Review
- Phosphatidic acid, phospholipase D and tumorigenesis.Advances in biological regulation · 2014Article
- Macrophage migration arrest due to a winning balance of Rac2/Sp1 repression over β-catenin-induced PLD expression.Journal of leukocyte biology · 2013Article
- Choline metabolism in malignant transformation.Nature reviews. Cancer · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The underlying mechanisms of oncogene-induced phospholipase D (PLD) activation have not been fully elucidated. The effect of the mutated-ras on PLD mRNA was examined using colon cancer cell lines as well as mock- and mutated ras-transfected NIH3T3 cells. Ras-mutation and activation were correlated, and cells with enhanced ras-activation showed increased PLD1 mRNA and protein. Analysis of the 5' PLD1 promoter using a representative cell line, DLD-1 and also mutated ras-NIH3T3, showed one Sp1-site as the important ras-responsible motif. Spl inhibition with mithramycin A and Spl siRNA inhibited PLD1 protein expression and its promoter activity. Sp1 but not Sp3 protein level and increased Sp1-motif binding activity were correlated with ras activation. Furthermore, overexpression of Sp1 in drosophila SL2 cells lacking Sp family proteins increased PLD1 promoter activity. EMSA and chromatin immunoprecipitation assay confirmed the importance of Sp1 protein binding to the Sp1-motif in ras-induced PLD1 mRNA expression.
Indexed as
Identifiers
19994725PMC11166399W407133466What 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.