Evidence map›Paper›PMID 19734943›Full record

ArticleOncogene2009

Mechanism of chemoresistance mediated by miR-140 in human osteosarcoma and colon cancer cells.

B Song, Y Wang, Y Xi, K Kudo, S Bruheim, G I Botchkina, E Gavin, Y Wan, A Formentini, M Kornmann and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 213 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
213citing papers in PubMed, 3 pooled it
9.1field-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

213 citing papers in PubMed, 3 syntheses or guidelines pooled it, 404 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Role of Exosomal Non-Coding RNAsMicroRNA (Shariqah, United Arab Emirates) · 2026
    Review
  5. Review
  6. Emerging roles of long non-coding RNAs in osteosarcoma.Frontiers in molecular biosciences · 2024
    Review
  7. Review
  8. HDAC-driven mechanisms in anticancer resistance: epigenetics and beyond.Cancer drug resistance (Alhambra, Calif.) · 2024
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
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  18. Article
  19. Review
  20. Article

153 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

12 authors at 7 institutions in 4 countries.

B SongTranslational Research Laboratory, Department of Pathology, Stony Brook University, Stony Brook, NY 11794-8691, USA.
Y Wang
Y Xi
K Kudo
S Bruheim
G I Botchkina
E Gavin
Y Wan
A Formentini
M Kornmann
O Fodstad
J Ju
Norwegian Cancer Society · NOStony Brook University · USUniversität Ulm · DEUSA Mitchell Cancer Institute · USWuhan University · CNStony Brook Medicine · USUniversity of South Alabama · US

Funding

Modulation of Serotonergic TransportersR01MH075020 · NIMH · GEORGETOWN UNIVERSITY · PI SIDHU, ANITA · 2007 to 2010
$1.3M
Novel Method for Isolating Actively Translated mRNAsR21CA114043 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI JU, JINGFANG · 2006 to 2007
$259k
NCI NIH HHS CA114043NCI NIH HHS R21 CA114043NIMH NIH HHS MH075020NIMH NIH HHS R01 MH075020
6 · The paper itself

Abstract

In this study, high-throughput microRNA (miRNA) expression analysis revealed that the expression of miR-140 was associated with chemosensitivity in osteosarcoma tumor xenografts. Tumor cells ectopically transfected with miR-140 were more resistant to methotrexate and 5-fluorouracil (5-FU). Overexpression of miR-140 inhibited cell proliferation in both osteosarcoma U-2 OS (wt-p53) and colon cancer HCT 116 (wt-p53) cell lines, but less so in osteosarcoma MG63 (mut-p53) and colon cancer HCT 116 (null-p53) cell lines. miR-140 induced p53 and p21 expression accompanied with G(1) and G(2) phase arrest only in cell lines containing wild type of p53. Histone deacetylase 4 (HDAC4) was confirmed to be one of the important targets of miR-140. The expression of endogenous miR-140 was significantly elevated in CD133(+hi)CD44(+hi) colon cancer stem-like cells that exhibit slow proliferating rate and chemoresistance. Blocking endogenous miR-140 by locked nucleic acid-modified anti-miR partially sensitized resistant colon cancer stem-like cells to 5-FU treatment. Taken together, our findings indicate that miR-140 is involved in the chemoresistance by reduced cell proliferation through G(1) and G(2) phase arrest mediated in part through the suppression of HDAC4. miR-140 may be a candidate target to develop novel therapeutic strategy to overcome drug resistance.

Indexed as

Antimetabolites, AntineoplasticBone NeoplasmsCell CycleCell ProliferationColonic NeoplasmsDrug Resistance, NeoplasmFluorouracilGene Expression Regulation, NeoplasticGenes, p53HCT116 CellsHumansMethotrexateMicroRNAsOsteosarcomaTransfectionTumor Cells, CulturedAntimetabolites, AntineoplasticFluorouracilMethotrexateMicroRNAsMirn140 microRNA, human

Identifiers

PMID19734943
PMCPMC2783211
OpenAlexW2088230889

What OpenQuestion holds

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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.