Evidence map›Paper›PMID 34868361›Full record

ArticleOncology letters2022

Long non-coding RNA MIR17HG sponges microRNA-21 to upregulate PTEN and regulate homoharringtonine-based chemoresistance of acute myeloid leukemia cells.

Jinhua Yan, Ling Yao, Ping Li, Guohe Wu, Xiaobin Lv

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. The cross-talk between GSK-3β, RKIP, and PTEN as potential targets for therapeutic implications in cancer: a comprehensive insight.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2026
    Review
  4. Review
  5. Unveiling immune mechanisms and potential biomarkers in intervertebral disc degeneration through integrated analysis.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025
    Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Cancer resistance via the downregulation of the tumor suppressorsExploration of targeted anti-tumor therapy · 2023
    Review
  11. Article
  12. Review
  13. 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 3 institutions in 1 country.

Jinhua YanDepartment of Hematology, The Third Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330008, P.R. China.
Ling YaoDepartment of Gastroenterology, The Third Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330008, P.R. China.
Ping LiDepartment of Hematology, The Third Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330008, P.R. China.
Guohe WuDepartment of Hematology, The Third Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330008, P.R. China.
Xiaobin LvJiangxi Key Laboratory of Cancer Metastasis and Precision Treatment, The Third Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330008, P.R. China.
Third Affiliated Hospital of Nanchang University · CNNanchang University · CNThird Hospital of Nanchang · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding (lnc)RNA MIR17HG has been identified as a oncogene whose roles in acute myeloid leukemia (AML) remain unclear. The present study aimed to investigate the role of lncRNA MIR17HG in AML. Differential expression of MIR17HG in AML was determined by reverse transcription-quantitative PCR. Overexpression assays and dual luciferase reporter assays were performed to determine the relationship between MIR17HG and microRNA (miR)-21, and apoptosis was analyzed by using an apoptosis assay. The results showed that the expression of MIR17HG was decreased in AML, which was further decreased following homoharringtonine (HHT)-based chemotherapy. Bioinformatics analysis predicted that miR-21 could bind with MIR17HG. However, miR-21 overexpression had no effect on the expression level of MIR17HG. Dual luciferase reporter assays were performed to verify the direct interaction between miR-21 and MIR17HG. In addition, overexpression of MIR17HG and miR-21 in AML cell lines up- and downregulated the expression level of PTEN, respectively. Furthermore, cell apoptosis showed that MIR17HG and PTEN overexpression enhanced cell apoptosis following cell treatment with HTT. However, miR-21 overexpression exerted the opposite effect, since it reversed the effects of MIR17HG and PTEN overexpression in AML cell apoptosis. In conclusion, the current study suggested that MIR17HG could regulate the miR-21/PTEN axis to modulate the chemoresistance of AML cells.

Indexed as

acute myeloid leukemiahomoharringtoninemicroRNA-21MIR17HGPTEN

Identifiers

PMID34868361
PMCPMC8630824
OpenAlexW3212337537

What OpenQuestion holds

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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.