Evidence map›Paper›PMID 32426817›Full record

ArticleBioscience reports2020

Knockdown of LncRNA CRNDE suppresses proliferation and P-glycoprotein-mediated multidrug resistance in acute myelocytic leukemia through the Wnt/β-catenin pathway.

Yiqing Kang, Suping Zhang, Weijie Cao, Dingming Wan, Ling Sun

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
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.

Yiqing KangDepartment of Hematology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou 450052, P.R. China.
Suping ZhangDepartment of Hematology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou 450052, P.R. China.
Weijie CaoDepartment of Hematology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou 450052, P.R. China.
Dingming WanDepartment of Hematology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou 450052, P.R. China.
Ling SunDepartment of Hematology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou 450052, P.R. China.
First Affiliated Hospital of Zhengzhou University · CNBeijing Red Cross Blood Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mechanisms involved in non-coding RNAs have been implicated in multidrug resistance (MDR) of acute myeloid leukemia (AML). Long non-coding RNA (lncRNAs) colorectal neoplasia differentially expressed (CRNDE) is reported to be involved in the malignant progression in AML. The purpose of the present study is to explore the roles and potential molecular mechanism of CRNDE in the MDR in AML. In our study, we confirmed that the expression of CRNDE was significantly up-regulated in patients with AML, especially in AML patients after adriamycin (ADR)-based chemotherapy. Spearman correlation analysis showed a positive correlation between the levels of CRNDE and MDR1 in AML patients after ADR-based chemotherapy. Moreover, CRNDE was up-regulated in AML cells, especially in ADR-resistant AML cells. Multidrug resistance protein 1 (MDR1)/p-glycoprotein (P-gp) levels were significantly increased in ADR-resistant AML cells, compared with parental AML cells. CRNDE down-regulation inhibited cell proliferation, promoted apoptosis, reduced Ki67 expression and enhanced cleaved caspase-3 expression in AML and ADR-resistant AML cells. In addition, CRNDE knockdown led to down-regulation of P-gp/MDR1, β-catenin, c-Myc and cyclinD1 expression, and enhanced the drug sensitivity to ADR in ADR-resistant AML cells. In conclusion, knockdown of CRNDE suppresses proliferation and P-gp-mediated MDR in ADR-resistant AML cells via inhibiting the Wnt/β-catenin pathway, suggesting that repression of CRNDE might be a therapeutic target to reverse MDR of ADR-resistant AML cells.

Indexed as

Drug Resistance, NeoplasmAntibiotics, AntineoplasticApoptosisATP Binding Cassette Transporter, Subfamily BCase-Control StudiesCell ProliferationDoxorubicinGene Expression Regulation, NeoplasticHL-60 CellsHumansLeukemia, Myeloid, AcuteRNA, Long NoncodingWnt Signaling PathwayABCB1 protein, humanAntibiotics, AntineoplasticATP Binding Cassette Transporter, Subfamily BCRNDE RNA, humanDoxorubicinRNA, Long Noncodingacute myelocytic leukemiaLncRNA CRNDEmultidrug resistanceP-glycoproteinWnt/β-catenin pathway

Identifiers

PMID32426817
PMCPMC7273914
OpenAlexW3027958029

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.