ArticlePloS one2011
The inhibitor of growth protein 5 (ING5) depends on INCA1 as a co-factor for its antiproliferative effects.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- The effects of flavonoid baicalein on miRNA expressions in cancer: a systematic review.Naunyn-Schmiedeberg's archives of pharmacology · 2025Pooled it
- Histone 3 Hyperacetylation and the Aggressive Behavior of Giant Cell Lesions.Cancer medicine · 2026Article
- OverlappING and DivergING roles of ING4 and ING5 in cancer, differentiation and development.Frontiers in cell and developmental biology · 2026Review
- TMEM11 regulates cardiomyocyte proliferation and cardiac repair via METTL1-mediated mCell death and differentiation · 2023Article
- The roles of ING5 in cancer: A tumor suppressor.Frontiers in cell and developmental biology · 2022Review
- Transcriptional Regulation of ING5 and its Suppressive Effects on Gastric Cancer.Frontiers in oncology · 2022Article
- Biological Functions of the ING Proteins.Cancers · 2019Review
- ING5 inhibits lung cancer invasion and epithelial-mesenchymal transition by inhibiting the WNT/β-catenin pathway.Thoracic cancer · 2019Article
- Potential role of chromatin remodeling factor genes in atrophic gastritis/gastric cancer risk.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2018Article
- ING5 activity in self-renewal of glioblastoma stem cells via calcium and follicle stimulating hormone pathways.Oncogene · 2018Article
- ING5 differentially regulates protein lysine acetylation and promotes p300 autoacetylation.Oncotarget · 2018Article
- ING5 is a Potential Target for Osteosarcoma Therapy.Technology in cancer research & treatment · 2018Article
- The roles of ING5 in gliomas: a good marker for tumorigenesis and a potential target for gene therapy.Oncotarget · 2017Article
- ING5 knockdown enhances migration and invasion of lung cancer cells by inducing EMT via EGFR/PI3K/Akt and IL-6/STAT3 signaling pathways.Oncotarget · 2017Article
- INGs are potential drug targets for cancer.Journal of cancer research and clinical oncology · 2017Review
- MiR-1307 promotes ovarian cancer cell chemoresistance by targeting the ING5 expression.Journal of ovarian research · 2017Article
- The down-regulated ING5 expression in lung cancer: a potential target of gene therapy.Oncotarget · 2016Article
- Article
- ING5 inhibits cancer aggressiveness via preventing EMT and is a potential prognostic biomarker for lung cancer.Oncotarget · 2015Article
- Article
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 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The proteins of the Inhibitor of Growth (ING) family are involved in multiple cellular functions such as cell cycle regulation, apoptosis, and chromatin remodeling. For ING5, its actual role in growth suppression and the necessary partners are not known. In a yeast-two-hybrid approach with human bone marrow derived cDNA, we identified ING5 as well as several other proteins as interaction partners of Inhibitor of cyclin A1 (INCA1) that we previously characterized as a novel interaction partner of cyclin A1/CDK2. ING5 expression in leukemic AML blasts was severely reduced compared to normal bone marrow. In line, ING5 inhibited bone marrow colony formation upon retroviral transduction. However, Inca1(-/-) bone marrow colony formation was not suppressed by ING5. In murine embryonic fibroblast (MEF) cells from Inca1(+/+) and Inca1(-/-) mice, overexpression of ING5 suppressed cell proliferation only in the presence of INCA1, while ING5 had no effect in Inca1(-/-) MEFs. ING5 overexpression induced a delay in S-phase progression, which required INCA1. Finally, ING5 overexpression enhanced Fas-induced apoptosis in Inca1(+/+) MEFs, while Inca1(-/-) MEFs were protected from Fas antibody-induced apoptosis. Taken together, these results indicate that ING5 is a growth suppressor with suppressed expression in AML whose functions depend on its interaction with INCA1.
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Registered trials
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