ArticleGene2009
Structure and promoter characterization of aldo-keto reductase family 1 B10 gene.
Article in Gene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Clinical value of AKR1B10 in hepatocellular carcinoma: A systematic review and meta-analysis.PloS one · 2022Pooled it
- Aldo-keto reductases: Role in cancer development and theranostics.Oncology research · 2024Review
- Propofol suppresses cell proliferation in gastric cancer cells through NRF2-mediated polyol pathway.Clinical and experimental pharmacology & physiology · 2022Article
- The Role of AKR1B10 in Physiology and Pathophysiology.Metabolites · 2021Review
- AKR1B10 expression predicts response of gastric cancer to neoadjuvant chemotherapy.Oncology letters · 2019Article
- Integrated analysis of the impact of age on genetic and clinical aspects of hepatocellular carcinoma.Aging · 2018Article
- Negative feedback loop between ZBTB7A and TGF-β in breast cancer.Oncology letters · 2017Article
- High expression of AKR1B10 predicts low risk of early tumor recurrence in patients with hepatitis B virus-related hepatocellular carcinoma.Scientific reports · 2017Article
- High expression of aldo-keto reductase 1B10 is an independent predictor of favorable prognosis in patients with hepatocellular carcinoma.Gut and liver · 2014Article
- AKR1B10 is induced by hyperglycaemia and lipopolysaccharide in patients with diabetic nephropathy.Cell stress & chaperones · 2014Article
- Up-regulated aldo-keto reductase family 1 member B10 in chronic hepatitis C: association with serum alpha-fetoprotein and hepatocellular carcinoma.Liver international : official journal of the International Association for the Study of the Liver · 2012Article
- Overexpression and oncogenic function of aldo-keto reductase family 1B10 (AKR1B10) in pancreatic carcinoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2012Article
- Aldo-Keto Reductase 1B10 and Its Role in Proliferation Capacity of Drug-Resistant Cancers.Frontiers in pharmacology · 2012Article
- AKR1B10 induces cell resistance to daunorubicin and idarubicin by reducing C13 ketonic group.Toxicology and applied pharmacology · 2011Article
- Pro-oncogene Pokemon promotes breast cancer progression by upregulating survivin expression.Breast cancer research : BCR · 2011Article
- Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Aldo-keto reductase family 1 member B10 (AKR1B10) is overexpressed in human hepatocellular carcinoma, lung squamous carcinoma, and lung adenocarcinoma in smokers. Our recent studies have showed that AKR1B10 plays a critical role in the growth and proliferation of cancer cells by detoxifying reactive carbonyls and regulating fatty acid biosynthesis. However, little is known about the regulatory mechanisms of AKR1B10 expression. In this study, we determined the structure of AKR1B10 gene and characterized its promoter. The results demonstrated that AKR1B10 consists of 10 exons and 9 introns, stretching approximately 13.8 kb. A 5'-RACE study determined the transcriptional start site of AKR1B10 at 320 bp upstream of the ATG translational start codon. A TATA-like (TAATAA) and a CAAT box are present from -145 to -140 bp and -193 to -190 bp upstream of the transcriptional start site, respectively. Motif analysis recognized multiple putative oncogenic and tumor suppressor protein binding sites in the AKR1B10 promoter, including c-Ets-1, C/EBP, AP-1, and p53, but osmolytic response elements were not found. A -4091 bp of the 5'-flanking fragment of the AKR1B10 gene was capable of driving GFP and luciferase reporter gene expression in HepG2 cells derived from human hepatocellular carcinoma; progressive 5'-deletions revealed that a -255 bp fragment possesses full promoter activity.
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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.