Evidence map›Paper›PMID 26107945›Full record

ArticlePloS one2015

MiR-133a Is Functionally Involved in Doxorubicin-Resistance in Breast Cancer Cells MCF-7 via Its Regulation of the Expression of Uncoupling Protein 2.

Yuan Yuan, Yu Feng Yao, Sai Nan Hu, Jin Gao, Li-Li Zhang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 24% 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, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Genes · 2026
    Review
  3. Review
  4. Does insulin make breast cancer cells resistant to doxorubicin toxicity?Naunyn-Schmiedeberg's archives of pharmacology · 2023
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Regulation of epithelial-mesenchymal transition through microRNAs: clinical and biological significance of microRNAs in breast cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  20. Article
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 1 institution in 1 country.

Yuan YuanDepartment of Chemotherapy, Jiangsu Cancer Hospital and Research Institute, Nanjing, Jiangsu, People's Republic of China.
Yu Feng YaoDepartment of Surgery, Jiangsu Cancer Hospital and Research Institute, Nanjing, Jiangsu, People's Republic of China.
Sai Nan HuDepartment of Chemotherapy, Jiangsu Cancer Hospital and Research Institute, Nanjing, Jiangsu, People's Republic of China.
Jin GaoDepartment of Chemotherapy, Jiangsu Cancer Hospital and Research Institute, Nanjing, Jiangsu, People's Republic of China.
Li-Li ZhangDepartment of Chemotherapy, Jiangsu Cancer Hospital and Research Institute, Nanjing, Jiangsu, People's Republic of China.
Jiangsu Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of novel targeted therapies holds promise for conquering chemotherapy resistance, which is one of the major hurdles in current breast cancer treatment. Previous studies indicate that mitochondria uncoupling protein 2 (UCP-2) is involved in the development of chemotherapy resistance in colon cancer and lung cancer cells. In the present study we found that lower level of miR133a is accompanied by increased expression of UCP-2 in Doxorubicin-resistant breast cancer cell cline MCF-7/Dox as compared with its parental cell line MCF-7. We postulated that miR133a might play a functional role in the development of Doxorubicin-resistant in breast cancer cells. In this study we showed that: 1) exogenous expression of miR133a in MCF-7/Dox cells can sensitize their reaction to the treatment of Doxorubicin, which is coincided with reduced expression of UCP-2; 2) knockdown of UCP-2 in MCF-7/Dox cells can also sensitize their reaction to the treatment of Doxorubicin; 3) intratumoral delivering of miR133a can restore Doxorubicin treatment response in Doxorubicin-resistant xenografts in vivo, which is concomitant with the decreased expression of UCP-2. These findings provided direct evidences that the miR133a/UCP-2 axis might play an essential role in the development of Doxorubicin-resistance in breast cancer cells, suggesting that the miR133a/UCP-2 signaling cohort could be served as a novel therapeutic target for the treatment of chemotherapy resistant in breast cancer.

Indexed as

Drug Resistance, NeoplasmGene Expression Regulation, NeoplasticAnimalsAntibiotics, AntineoplasticCell SurvivalDoxorubicinFemaleHumansIon ChannelsMammary Neoplasms, ExperimentalMCF-7 CellsMiceMice, NudeMicroRNAsMitochondrial ProteinsNeoplasm TransplantationAntibiotics, AntineoplasticDoxorubicinIon ChannelsMicroRNAsMIRN133 microRNA, humanMitochondrial ProteinsUCP2 protein, humanUcp2 protein, mouseUncoupling Protein 2

Identifiers

PMID26107945
PMCPMC4481265
OpenAlexW1176569914

What OpenQuestion holds

Textmetadata
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.