Evidence map›Paper›PMID 25867061›Full record

Trial reportOncogene2016

MiRNA-621 sensitizes breast cancer to chemotherapy by suppressing FBXO11 and enhancing p53 activity.

J Xue, Y Chi, Y Chen, S Huang, X Ye, J Niu, W Wang, L M Pfeffer, Z-M Shao, Z-H Wu and 1 more

Open access · hybridAbstract readClinical Trial, Phase II
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Genetic variations in tumor-suppressor miRNA-encoding genes and their target genes: focus on breast cancer development and possible therapeutic strategies.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Review
  10. Article
  11. FBXW7 in breast cancer: mechanism of action and therapeutic potential.Journal of experimental & clinical cancer research : CR · 2023
    Review
  12. Article
  13. Review
  14. FBXO11 constitutes a major negative regulator of MHC class II through ubiquitin-dependent proteasomal degradation of CIITA.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  15. Review
  16. Article
  17. Review
  18. RNAi-Based Therapeutics and Novel RNA Bioengineering Technologies.The Journal of pharmacology and experimental therapeutics · 2023
    Review
  19. Article
  20. Article

11 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

11 authors at 5 institutions in 2 countries.

J XueDepartment of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Y ChiDepartment of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Y ChenDepartment of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
S HuangDepartment of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
X YeInstitut Mérieux Laboratory, Fudan University Shanghai Cancer Center, Shanghai, China.
J NiuCenter for Cancer Research, University of Tennessee Health Science Center, Memphis, TN, USA.
W WangCenter for Cancer Research, University of Tennessee Health Science Center, Memphis, TN, USA.
L M PfefferCenter for Cancer Research, University of Tennessee Health Science Center, Memphis, TN, USA.
Z-M ShaoDepartment of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Z-H WuCenter for Cancer Research, University of Tennessee Health Science Center, Memphis, TN, USA.
J WuDepartment of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Fudan University Shanghai Cancer Center · CNCenter for Cancer Research · USUniversity of Tennessee Health Science Center · USShanghai Medical College of Fudan University · CNWenzhou Medical University · CN

Funding

Genotoxic NF-kB Signaling in CancerR01CA149251 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI WU, ZHAOHUI · 2011 to 2015
$1.5M
NCI NIH HHS R01 CA149251NCI NIH HHS R01CA149251
6 · The paper itself

Abstract

MicroRNAs (miRNAs) have been demonstrated to have critical roles in regulating cancer cell proliferation, survival and sensitivity to chemotherapy. The potential application of using miRNAs to predict therapeutic response to cancer treatment holds high promise, but miRNAs with predictive value remain to be identified and underlying mechanisms have not been completely understood. Here, we show a strong correlation between miR-621 expression and chemosensitivity to paclitaxel plus carboplatin (PTX/CBP) regimen, an effective neoadjuvant chemotherapy for breast cancer patients. High level of miR-621 predicts better response to PTX/CBP regimen neoadjuvant chemotherapy in breast cancer patients, who also tend to achieve pathological complete response. Ectopic overexpression of miR-621 promoted apoptosis and increased chemosensitivity to PTX and CBP both in cultured breast cancer cells and in xenograft tumor model. We further show that FBXO11 is a direct functional target of miR-621 and miR-621 level is negatively correlated with FBXO11 expression in breast cancer patients. Ectopic expression of FBXO11 attenuated increased apoptosis in breast cancer cells overexpressing miR-621 upon PTX or CBP treatment. Consistently, high FBXO11 expression significantly correlated with poor survival in breast cancer patients. Mechanistically, we found in breast cancer cells FBXO11 interacts with p53 and promotes its neddylation, which suppressed the p53 transactivity. Accordingly, miR-621-dependent FBXO11 suppression enhanced p53 activity and increased apoptosis in breast cancer cells exposed to chemotherapeutics. Taken together, our data suggest that miR-621 enhances chemosensitivity of breast cancer cells to PTX/CBP chemotherapy by suppressing FBXO11-dependent inhibition of p53. miR-621 may serve as a predictive biomarker and a potential therapeutic target in breast cancer treatment.

Indexed as

AdultAnimalsAntineoplastic Combined Chemotherapy ProtocolsBreast NeoplasmsCarboplatinCell Line, TumorF-Box ProteinsFemaleGene Expression Regulation, NeoplasticHumansMice, Inbred BALB CMicroRNAsMiddle AgedPaclitaxelProtein-Arginine N-MethyltransferasesTreatment OutcomeCarboplatinF-Box ProteinsFBXO11 protein, humanMicroRNAsMIRN621 microRNA, humanPaclitaxelProtein-Arginine N-MethyltransferasesTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID25867061
PMCPMC4603999
OpenAlexW1976285590

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.