ArticleMolecular biology of the cell2009
Induction of Dlk1 by PTTG1 inhibits adipocyte differentiation and correlates with malignant transformation.
Article in Molecular biology of the cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Inhibition of PTTG1 suppresses proliferation and promotes differentiation of neuroblastoma cells by inducing autophagy.Pediatric surgery international · 2025Article
- DLK1 Distinguishes Subsets of NF1-Associated Malignant Peripheral Nerve Sheath Tumors with Divergent Molecular Signatures.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- Transcriptomics of Subcutaneous Tissue of Lipedema Identified Differentially Expressed Genes Involved in Adipogenesis, Inflammation, and Pain.Plastic and reconstructive surgery. Global open · 2024Article
- Transcriptional response to an alternative diet on liver, muscle, and rumen of beef cattle.Scientific reports · 2024Article
- Pituitary Tumor-Transforming Gene 1/Delta like Non-Canonical Notch Ligand 1 Signaling in Chronic Liver Diseases.International journal of molecular sciences · 2022Review
- The pituitary tumour-transforming gene 1/delta-like homologue 1 pathway plays a key role in liver fibrogenesis.Liver international : official journal of the International Association for the Study of the Liver · 2022Article
- Simvastatin Suppresses Human Breast Cancer Cell Invasion by Decreasing the Expression of Pituitary Tumor-Transforming Gene 1.Frontiers in pharmacology · 2020Article
- Long noncoding RNA CCAT2 is activated by E2F1 and exerts oncogenic properties by interacting with PTTG1 in pituitary adenomas.American journal of cancer research · 2018Article
- Delta-like 1 homolog in Capra hircus: molecular characteristics, expression pattern and phylogeny.Molecular biology reports · 2016Article
- A genetic platform to model sarcomagenesis from primary adult mesenchymal stem cells.Cancer discovery · 2015Article
- An inhibitory role of progerin in the gene induction network of adipocyte differentiation from iPS cells.Aging · 2013Article
- Down-regulation of the oncogene PTTG1 via the KLF6 tumor suppressor during induction of myeloid differentiation.PloS one · 2013Article
- Meat Science and Muscle Biology Symposium: stem cell niche and postnatal muscle growth.Journal of animal science · 2012Review
- Silencing of the imprinted DLK1-MEG3 locus in human clinically nonfunctioning pituitary adenomas.The American journal of pathology · 2011Article
- Article
- Association analyses identify six new psoriasis susceptibility loci in the Chinese population.Nature genetics · 2010Article
- Isolation and characterization of novel pituitary tumor related genes: a cDNA representational difference approach.Molecular and cellular endocrinology · 2010Review
- BZL101, a phytochemical extract from the Scutellaria barbata plant, disrupts proliferation of human breast and prostate cancer cells through distinct mechanisms dependent on the cancer cell phenotype.Cancer biology & therapy · 2010Article
- A distinct spectrum of copy number aberrations in pediatric high-grade gliomas.Clinical cancer research : an official journal of the American Association for Cancer Research · 2010Article
- Therapeutic efficacy of combined vaccination against tumor pericyte-associated antigens DLK1 and DLK2 in mice.OncoimmunologyArticle
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pituitary tumor-transforming gene-1 (PTTG1) is an oncogene highly expressed in a variety of endocrine, as well as nonendocrine-related cancers. Several tumorigenic mechanisms for PTTG1 have been proposed, one of the best characterized being its capacity to act as a transcriptional activator. To identify novel downstream target genes, we have established cell lines with inducible expression of PTTG1 and a differential display approach to analyze gene expression changes after PTTG1 induction. We identified dlk1 (also known as pref-1) as one of the most abundantly expressed PTTG1 targets. Dlk1 is known to participate in several differentiation processes, including adipogenesis, adrenal gland development, and wound healing. Dlk1 is also highly expressed in neuroendocrine tumors. Here, we show that PTTG1 overexpression inhibits adipogenesis in 3T3-L1 cells and that this effect is accomplished by promoting the stability and accumulation of Dlk1 mRNA, supporting a role for PTTG1 in posttranscriptional regulation. Moreover, both pttg1 and dlk1 genes show concomitant expression in fetal liver and placenta, as well as in pituitary adenomas, breast adenocarcinomas, and neuroblastomas, suggesting that PTTG1 and DLK1 are involved in cell differentiation and transformation.
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.