Evidence map›Paper›PMID 17404574›Full record

ArticleOncogene2007

mir-29 regulates Mcl-1 protein expression and apoptosis.

J L Mott, S Kobayashi, S F Bronk, G J Gores

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 447 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
447citing papers in PubMed, 2 pooled it
25.2field-weighted citation impact, top 1% 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

447 citing papers in PubMed, 2 syntheses or guidelines pooled it, 827 citations in OpenAlex.

  1. Pooled it
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  13. Review
  14. The Role of microRNAs Related to Apoptosis forInternational journal of molecular sciences · 2024
    Article
  15. Article
  16. Noncoding RNAs: the crucial role of programmed cell death in osteoporosis.Frontiers in cell and developmental biology · 2024
    Review
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  18. Review
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  20. Article

387 more citing papers are in PubMed but not listed here.

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.

J L MottDivision of Gastroenterology and Hepatology, Miles and Shirley Fiterman Center for Digestive Diseases, Mayo Clinic College of Medicine, Rochester, MN, USA.
S Kobayashi
S F Bronk
G J Gores
Mayo Clinic in Arizona · US

Funding

Mechanisms of Carcinogenesis in Biliary EpitheliaR01DK059427 · NIDDK · MAYO CLINIC ROCHESTER · PI GORES, GREGORY J. · 2001 to 2016
$4.3M
Mechanisms of Carcinogenesis in Biliary EpitheliaR56DK059427 · NIDDK · MAYO CLINIC ROCHESTER · PI GORES, GREGORY J. · 2006 to 2006
$243k
NIDDK NIH HHS DK59427NIDDK NIH HHS R01 DK059427NIDDK NIH HHS R56 DK059427
6 · The paper itself

Abstract

Cellular expression of Mcl-1, an anti-apoptotic Bcl-2 family member, is tightly regulated. Recently, Bcl-2 expression was shown to be regulated by microRNAs, small endogenous RNA molecules that regulate protein expression through sequence-specific interaction with messenger RNA. By analogy, we reasoned that Mcl-1 expression may also be regulated by microRNAs. We chose human immortalized, but non-malignant, H69 cholangiocyte and malignant KMCH cholangiocarcinoma cell lines for these studies, because Mcl-1 is dysregulated in cells with the malignant phenotype. By in silico analysis, we identified a putative target site in the Mcl-1 mRNA for the mir-29 family, and found that mir-29b was highly expressed in cholangiocytes. Interestingly, mir-29b was downregulated in malignant cells, consistent with Mcl-1 protein upregulation. Enforced mir-29b expression reduced Mcl-1 protein expression in KMCH cells. This effect was direct, as mir-29b negatively regulated the expression of an Mcl-1 3' untranslated region (UTR)-based reporter construct. Enforced mir-29b expression reduced Mcl-1 cellular protein levels and sensitized the cancer cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) cytotoxicity. Transfection of non-malignant cells (that express high levels of mir-29) with a locked-nucleic acid antagonist of mir-29b increased Mcl-1 levels and reduced TRAIL-mediated apoptosis. Thus mir-29 is an endogenous regulator of Mcl-1 protein expression, and thereby, apoptosis.

Indexed as

ApoptosisCell Line, TransformedCell Line, TumorGene Expression Regulation, NeoplasticHumansMicroRNAsMyeloid Cell Leukemia Sequence 1 ProteinNeoplasm ProteinsProto-Oncogene Proteins c-bcl-2MicroRNAsMyeloid Cell Leukemia Sequence 1 ProteinNeoplasm ProteinsProto-Oncogene Proteins c-bcl-2

Identifiers

PMID17404574
PMCPMC2432524
OpenAlexW1966116761

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.