Evidence map›Paper›PMID 25980495›Full record

ArticleOncotarget2015

Inhibition of colorectal cancer stem cell survival and invasive potential by hsa-miR-140-5p mediated suppression of Smad2 and autophagy.

Haiyan Zhai, Andrew Fesler, Yufeng Ba, Song Wu, Jingfang Ju

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 2 pooled it
6.3field-weighted citation impact, top 2% 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

67 citing papers in PubMed, 2 syntheses or guidelines pooled it, 139 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  6. Review
  7. Development of 5-FU-modified tumor suppressor microRNAs as a platform for novel microRNA-based cancer therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  8. Article
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  11. Virus, Exosome, and MicroRNA: New Insights into Autophagy.Advances in experimental medicine and biology · 2022
    Article
  12. Article
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  14. Article
  15. Article
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  20. The Emerging Roles of Autophagy-Related MicroRNAs in Cancer.International journal of biological sciences · 2021
    Review

7 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

5 authors at 2 institutions in 2 countries.

Haiyan ZhaiTranslational Research Laboratory, Department of Pathology, Stony Brook University, Stony Brook, NY 11794 USA.
Andrew FeslerTranslational Research Laboratory, Department of Pathology, Stony Brook University, Stony Brook, NY 11794 USA.
Yufeng BaDepartment of Thoracic Surgery, The Cancer Hospital of Henan, Zhengzhou, Henan 450008 China.
Song WuDepartment of Applied Mathematics and Statistics, Stony Brook University, Stony Brook, NY 11794 USA.
Jingfang JuTranslational Research Laboratory, Department of Pathology, Stony Brook University, Stony Brook, NY 11794 USA.
Stony Brook University · USHenan Cancer Hospital · CN

Funding

Molecular Mechanism of miR-140 in Colon CancerR01CA155019 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI JU, JINGFANG · 2011 to 2014
$1.5M
Identification of post-transcriptionally regulated targets by TrIP-Chip/SeqR33CA147966 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI JU, JINGFANG · 2011 to 2013
$674k
NCI NIH HHS R01 CA155019NCI NIH HHS R01CA155019NCI NIH HHS R33 CA147966NCI NIH HHS R33CA147966
6 · The paper itself

Abstract

Colorectal cancer (CRC) is the third highest mortality cancer in the United States and frequently metastasizes to liver and lung. Smad2 is a key element downstream of the TGF-β signaling pathway to regulate cancer metastasis by promoting epithelial to mesenchymal transition and maintaining the cancer stem cell (CSC) phenotype. In this study, we show that hsa-miR-140-5p directly targets Smad2 and overexpression of hsa-miR-140-5p in CRC cell lines decreases Smad2 expression levels, leading decreased cell invasion and proliferation, and increasing cell cycle arrest. Ectopic expression of hsa-miR-140-5p in colorectal CSCs inhibited CSC growth and sphere formation in vitro by disrupting autophagy. We have systematically identified targets of hsa-miR-140-5p involved in autophagy. Furthermore, overexpression of hsa-miR-140-5p in CSCs abolished tumor formation and metastasis in vivo. In addition, there is a progressive loss of hsa-miR-140-5p expression from normal colorectal mucosa to primary tumor tissues, with further reduction in liver metastatic tissues. Higher hsa-miR-140 expression is significantly correlated with better survival in stage III and IV colorectal cancer patients.The functional and clinical significance of hsa-miR-140-5p suggests that it is a key regulator in CRC progression and metastasis, and may have potential as a novel therapeutic molecule to treat CRC.

Indexed as

AutophagyAnimalsCell Cycle CheckpointsCell MovementCell ProliferationCell SurvivalColorectal NeoplasmsGene Expression Regulation, NeoplasticGenetic TherapyHCT116 CellsHumansLiver NeoplasmsMice, Inbred NODMice, SCIDMicroRNAsNeoplasm InvasivenessMicroRNAsMirn140 microRNA, humanSmad2 ProteinSMAD2 protein, humanautophagycolon cancer stem cellhsa-miR-140-5pmetastasisSmad2

Identifiers

PMID25980495
PMCPMC4637317
OpenAlexW2107386180

What OpenQuestion holds

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LicenceCC BY
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.