ArticleCancer letters2014
Knockdown or inhibition of aldo-keto reductase 1B10 inhibits pancreatic carcinoma growth via modulating Kras-E-cadherin pathway.
Article in Cancer letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
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Who cites it
28 citing papers in PubMed, 49 citations in OpenAlex.
- AKR1B10 reprograms neutrophils by histone lactylation to foster immune evasion in KRASJournal of experimental & clinical cancer research : CR · 2026Article
- AKR1B10 dictates c-Myc stability to suppress colorectal cancer metastasis via PP2A nitration.Science advances · 2025Article
- Complex Inhibitory Activity of Pentacyclic Triterpenoids against Cutaneous Melanoma In Vitro and In Vivo: A Literature Review and Reconstruction of Their Melanoma-Related Protein Interactome.ACS pharmacology & translational science · 2024Review
- AKR1B10 and digestive tumors development: a review.Frontiers in immunology · 2024Review
- Aldo-keto reductases: Role in cancer development and theranostics.Oncology research · 2024Review
- Diagnostic value of aldo‑keto reductase family 1 member B10 in human nasopharyngeal carcinoma.Molecular and clinical oncology · 2023Article
- Serum AKR1B10 as an indicator of unfavorable survival of hepatocellular carcinoma.Journal of gastroenterology · 2023Article
- Nimbolide Inhibits SOD2 to Control Pancreatic Ductal Adenocarcinoma Growth and Metastasis.Antioxidants (Basel, Switzerland) · 2023Article
- A Novel Cuproptosis-Associated Gene Signature to Predict Prognosis in Patients with Pancreatic Cancer.BioMed research international · 2023Article
- The role of metabolic reprogramming in pancreatic cancer chemoresistance.Frontiers in pharmacology · 2022Review
- CBX7 suppresses urinary bladder cancer progression via modulating AKR1B10-ERK signaling.Cell death & disease · 2021Article
- The Role of AKR1B10 in Physiology and Pathophysiology.Metabolites · 2021Review
- Regulation Network and Prognostic Significance of Aldo-Keto Reductase (AKR) Superfamily Genes in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2021Article
- Aldo Keto Reductases AKR1B1 and AKR1B10 in Cancer: Molecular Mechanisms and Signaling Networks.Advances in experimental medicine and biology · 2021Review
- Oncogenic function of TRIM2 in pancreatic cancer by activating ROS-related NRF2/ITGB7/FAK axis.Oncogene · 2020Observational
- Metabolism of pancreatic cancer: paving the way to better anticancer strategies.Molecular cancer · 2020Review
- Relief of Cadmium-Induced Intestinal Motility Disorder in Mice byFrontiers in immunology · 2020Article
- Inhibition of Pancreatic Carcinoma Growth Through Enhancing ω-3 Epoxy Polyunsaturated Fatty Acid Profile by Inhibition of Soluble Epoxide Hydrolase.Anticancer research · 2019Article
- The hop-derived compounds xanthohumol, isoxanthohumol and 8-prenylnaringenin are tight-binding inhibitors of human aldo-keto reductases 1B1 and 1B10.Journal of enzyme inhibition and medicinal chemistry · 2018Article
- Selective Inhibition of Human AKR1B10 byMolecules (Basel, Switzerland) · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Aldo-keto reductase 1B10 (AKR1B10) has relatively specific lipid substrates including carbonyls, retinal and farnesal/geranylgeranial. Metabolizing these lipid substrates appears crucial to carcinogenesis, particularly for farnesal/geranylgeranial that involves protein prenylation. Mutant Kras is a most common active oncogene in pancreatic cancer, and its activation requires protein prenylation. To directly determine the role of AKR1B10 in pancreatic carcinogenesis, we knocked down AKR1B10 in CD18 human pancreatic carcinoma cells using shRNA approach. Silencing AKR1B10 resulted in a significant inhibition of anchor-dependent growth (knockdown cells vs. vector-control cells: 67 ± 9.5 colonies/HPF vs. 170 ± 3.7 colonies/HPF, p < 0.01), invasion index (0.27 vs. 1.00, p < 0.05), and cell migration (at 16 hours 9.2 ± 1.2% vs. 14.0 ± 1.8%, at 24 hours 21.0 ± 1.1% vs. 30.5 ± 3.5%, and at 48 hours 51.9 ± 5.7% vs. 88.9 ± 3.0%, p < 0.01). Inhibition of AKR1B10 by oleanolic acid (OA) showed a dose-dependent inhibition of cell growth with IC50 at 30 µM. Kras pull-down and Western blot analysis revealed a significant down-regulation of active form Kras and phosphorylated C-Raf, and Erk, as well as an up-regulation of E-cadherin. A significant reduction of in vivo tumor growth was observed in nude mice implanted with the CD18 pancreatic carcinoma cells with AKR1B10 knockdown (tumor weight: 0.25 ± 0.06 g vs. 0.52 ± 0.07 g, p = 0.01), and with OA treatment (tumor weight: 0.35 ± 0.05 g vs. 0.52 ± 0.07 g, p = 0.05). Our findings indicate AKR1B10 is a unique enzyme involved in pancreatic carcinogenesis via modulation of the Kras-E-cadherin pathway.
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