Evidence map›Paper›PMID 25213664›Full record

ArticleCancer gene therapy2014

The malignancy suppression role of miR-23a by targeting the BCR/ABL oncogene in chromic myeloid leukemia.

Z Xishan, L Xianjun, L Ziying, C Guangxin, L Gang

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Cancer gene therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Non-Coding RNAs Are Implicit in Chronic Myeloid Leukemia Therapy Resistance.International journal of molecular sciences · 2022
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. MicroRNAs as prognostic biomarker and relapse indicator in leukemia.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2017
    Review
  14. Review
  15. Article
  16. miRNA143 Induces K562 Cell Apoptosis Through Downregulating BCR-ABL.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Article
  17. Review
  18. Article
  19. Article
  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 2 institutions in 1 country.

Z XishanClinical Research Center, Affiliated Hospital of Guangdong Medical College, Guangdong province, China.
L XianjunDepartment of Nuclear Medicine, Weifang People's Hospital, Weifang, Shandong, P.R. China.
L ZiyingClinical Research Center, Affiliated Hospital of Guangdong Medical College, Guangdong province, China.
C GuangxinDepartment of Nuclear Medicine, Weifang People's Hospital, Weifang, Shandong, P.R. China.
L GangClinical Research Center, Affiliated Hospital of Guangdong Medical College, Guangdong province, China.
Guangdong Medical College · CNWeifang People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of this study was to investigate the role and mechanism of miR-23a in the regulation of BCR/ABL and to provide a new prognostic biomarker for chronic myeloid leukemia (CML). The expression levels of miR-23a and BCR/ABL were assessed in 42 newly diagnosed CML patients, 37 CML patients in first complete remission and 25 healthy controls. Quantitative real-time PCR, western blot analysis and colony formation assay were used to evaluate changes induced by overexpression or inhibition of miR-23a or BCR/ABL. MiR-23a mimic or negative control mimic was transfected into a CML cell line (K562) and two lung cancer cell lines (H157 and SKMES1) using Lipofectamine 2000, and the cells were used for real-time reverse transcription-PCR (RT-PCR) and western blot analysis. We found that the downregulation of miR-23a expression was a frequent event in both leukemia cell lines and primary leukemic cells from patients with de novo CML. The microarray results showed that most of the CML patients expressed high levels of BCR/ABL and low levels of miR-23a. Real-time RT-PCR and western blot analysis showed that the BCR/ABL levels in miR-23a-transfected cells were lower than those in the control groups. Ectopic expression of miR-23a in K562 cells led to cellular senescence. Moreover, when K562 cells were treated with 5-aza-2'-deoxycytidine, a DNA methylation inhibitor, BCR/ABL expression was upregulated, which indicates epigenetic silencing of miR-23a in leukemic cells. BCR/ABL and miR-23a expressions were inversely related to CML, and BCR/ABL expression was regulated by miR-23a in leukemic cells. The epigenetic silencing of miR-23a led to derepression of BCR/ABL expression, and consequently contributes to CML development and progression.

Indexed as

RNA Interference3' Untranslated RegionsAdolescentAdultAgedAzacitidineBone MarrowBone Marrow CellsCell Line, TumorCellular SenescenceFemaleFusion Proteins, bcr-ablGene Expression Regulation, LeukemicHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMale3' Untranslated RegionsAzacitidineFusion Proteins, bcr-ablMatrix Metalloproteinase 9MicroRNAsMIRN23a microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID25213664
OpenAlexW1992423779

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.