ArticleThe American journal of pathology2006
Growth regulation via insulin-like growth factor binding protein-4 and -2 in association with mutant K-ras in lung epithelia.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 85 citations in OpenAlex.
- Early Growth Response Factor 4 (EGR4) Expression in Gut Tissues and Regional Lymph Nodes of Cattle with Different Types of Paratuberculosis-Associated Lesions: Potential Role of EGR4 in Resilience to Paratuberculosis.Animals : an open access journal from MDPI · 2025Article
- Quantification of putative ovarian cancer serum protein biomarkers using a multiplexed targeted mass spectrometry assay.Clinical proteomics · 2024Article
- FGF1 ameliorates obesity-associated hepatic steatosis by reversing IGFBP2 hypermethylation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Green tea extract and hydroxyl-chloroquine combination enhances apoptosis in A549 non-small cell lung cancer cells.Bioinformation · 2023Article
- Anticancer mechanism of breviscapine in non-small cell lung cancer A549 cells acts via ROS-mediated upregulation of IGFBP4.Journal of thoracic disease · 2021Article
- Potential Role of Insulin Growth-Factor-Binding Protein 2 as Therapeutic Target for Obesity-Related Insulin Resistance.International journal of molecular sciences · 2021Review
- Overexpression of lncRNA IGFBP4-1 reprograms energy metabolism to promote lung cancer progression.Molecular cancer · 2017Article
- Analysis of Purified Pancreatic Islet Beta and Alpha Cell Transcriptomes Reveals 11β-Hydroxysteroid Dehydrogenase (Hsd11b1) as a Novel Disallowed Gene.Frontiers in genetics · 2017Article
- New insights into estrogenic regulation ofJournal of biomedical research · 2016Article
- IGF-Binding Protein 2 - Oncogene or Tumor Suppressor?Frontiers in endocrinology · 2015Review
- Is insulin-like growth factor binding protein 2 associated with metastasis in lung cancer?Clinical & experimental metastasis · 2014Article
- Maternal nutritional history modulates the hepatic IGF-IGFBP axis in adult male rat offspring.Endocrine · 2014Article
- Smoking attenuates transforming growth factor-β-mediated tumor suppression function through downregulation of Smad3 in lung cancer.Cancer prevention research (Philadelphia, Pa.) · 2012Article
- Early growth response-1 induces and enhances vascular endothelial growth factor-A expression in lung cancer cells.The American journal of pathology · 2010Article
- Role of insulin-like growth factor binding protein 2 in lung adenocarcinoma: IGF-independent antiapoptotic effect via caspase-3.The American journal of pathology · 2010Article
- Down-regulation of FXYD3 expression in human lung cancers: its mechanism and potential role in carcinogenesis.The American journal of pathology · 2009Article
- Neuroendocrine cancer-specific up-regulating mechanism of insulin-like growth factor binding protein-2 in small cell lung cancer.The American journal of pathology · 2009Article
- Down-regulation of DUSP6 expression in lung cancer: its mechanism and potential role in carcinogenesis.The American journal of pathology · 2009Article
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 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gain-of-function point mutations in K-ras affect early events in pulmonary bronchioloalveolar carcinoma. We investigated altered mRNA expression on K-Ras activation in human peripheral lung epithelial cells (HPL1A) using oligonucleotide microarrays. Mutated K-Ras stably expressed in HPL1A accelerated cell growth and induced the expression of insulin-like growth factor (IGF)-binding protein (IGFBP)-4 and IGFBP-2, which modulate cell growth via IGF. Other lung epithelial cell lines (NHBE and HPL1D) revealed the same phenomena as HPL1A by mutated K-ras transgene. Lung cancer cell growth was also accelerated by mutated K-ras gene transduction, whereas IGFBP-4/2 induction was weaker compared with mutated K-Ras-expressing lung epithelial cells. To understand the differences in IGFBP-4/2 inducibility via K-Ras-activated signaling between nonneoplastic lung epithelia and lung carcinoma, we addressed the mechanisms of IGFBP-4/2 transcriptional activation. Our results revealed that Egr-1, which is induced on activation of Ras-mitogen-activated protein kinase signaling, is crucial for transactivation of IGFBP-4/2. Furthermore, IGFBP-4 and IGFBP-2 promoters were often hypermethylated in lung carcinoma, yielding low basal expression/weak induction of IGFBP-4/2. These findings suggest that continuous K-Ras activation accelerates cell growth and evokes a feedback system through IGFBP-4/2 to prevent excessive growth. Moreover, this growth regulation is disrupted in lung cancers because of promoter hypermethylation of IGFBP-4/2 genes.
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.