Evidence map›Paper›PMID 22978663›Full record

ArticleAntioxidants & redox signaling2013

Aldose reductase inhibition prevents colon cancer growth by restoring phosphatase and tensin homolog through modulation of miR-21 and FOXO3a.

Ashish Saxena, Ravinder Tammali, Kota V Ramana, Satish K Srivastava

Open access · greenAbstract read
In one paragraph

Article in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 20% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Identifying the Soybean microRNAs Related toInternational journal of molecular sciences · 2023
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  17. Gedunin abrogates aldose reductase, PI3K/Akt/mToR, and NF-κB signaling pathways to inhibit angiogenesis in a hamster model of oral carcinogenesis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Ashish SaxenaDepartment of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas 77555, USA.
Ravinder Tammali
Kota V Ramana
Satish K Srivastava
The University of Texas Medical Branch at Galveston · US

Funding

Role of Aldose Reductase in Diabetic ComplicationsR37DK036118 · NIDDK · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI SRIVASTAVA, SATISH K · 2003 to 2013
$4.1M
Chemoprevention of Colorectal Cancer by Aldose Reductase InhibitionR01CA129383 · NCI · UNIVERSITY OF TEXAS MED BR GALVESTON · PI RAMANA, KOTA VENKATA · 2008 to 2017
$3.1M
NCI NIH HHS CA129383NCI NIH HHS R01 CA129383NIDDK NIH HHS R37 DK036118
6 · The paper itself

Abstract

aimsWe have shown earlier that inhibition of aldose reductase (AR), an oxidative stress-response protein, prevents colon cancer cell growth in vitro and in vivo. Changes in microribonucleic acid (miR) expression can contribute to cancer by modulating the functional expression of critical genes involved in cancer growth and metastasis. However, the molecular mechanisms by which AR regulates miR expression and their dependent mitogenic effects in cancer cells are not known. Therefore, we investigated how AR regulates growth factor-induced expression of miRs and growth of colon cancer cells.

resultsInhibition of AR significantly downregulated growth factor-induced miR-21 expression in human colon cancer cells, HT29, SW480, and Caco-2. Further, AR inhibition also increased phosphatase and tensin homolog (PTEN) (a direct target of miR-21) and forkhead box O3A (FOXO3a) in colon cancer cells. Our results obtained with HT29 cells ablated with FOXO3a siRNA showed increased activator protein-1 (AP-1) activation and miR-21 expression, indicating that FOXO3a represses miR-21 via AP-1 inactivation. Inhibition of AR also prevented the epidermal growth factor-induced phosphorylation of phosphatidylinositol 3-kinase (PI3K), serine/threonine kinase (AKT), c-Jun, c-Fos, PTEN, and FOXO3a, and deoxyribonucleic acid (DNA)-binding activity of AP-1. More importantly, in human colon adenocarcinoma xenograft tissues, miR-21 expression was lower, and PTEN and FOXO3a levels were significantly higher in AR inhibitor-treated mice compared to controls. INNOVATION: These findings demonstrate a novel role of AR in the regulation of miR-21 and its target PTEN in growth factor-induced colon cancer cell growth.

conclusionsCollectively, these results show a novel role of AR in mediation of growth factor-induced colon cancer growth by modulating miR-21, PTEN, and FOXO3a expression through reactive oxygen species (ROS)/PI3K/AKT/AP-1.

Indexed as

Aldehyde ReductaseAnimalsCell Line, TumorColonic NeoplasmsDisease Models, AnimalForkhead Box Protein O3Forkhead Transcription FactorsGene Expression ProfilingGene Expression Regulation, NeoplasticHT29 CellsHumansIntercellular Signaling Peptides and ProteinsMiceMicroRNAsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAldehyde ReductaseForkhead Box Protein O3Forkhead Transcription FactorsFOXO3 protein, humanIntercellular Signaling Peptides and ProteinsMicroRNAsMIRN21 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseTranscription Factor AP-1

Identifiers

PMID22978663
PMCPMC3584509
OpenAlexW1988945136

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.