Evidence map›Paper›PMID 32782437›Full record

ArticleCancer cell international2020

Tanshinone IIA regulates human AML cell proliferation, cell cycle, and apoptosis through miR-497-5p/AKT3 axis.

Zi-Yuan Nie, Ming-Hui Zhao, Bao-Qian Cheng, Rong-Fang Pan, Tian-Rui Wang, Yan Qin, Xue-Jun Zhang

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  7. Anti-CLL1 liposome loaded with miR-497-5p and venetoclax as a novel therapeutic strategy in acute myeloid leukemia.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  8. Review
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  15. Frontiers in pharmacology · 2022
    Review
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  19. CircMYC regulates the mitochondrial respiration and cell viabilityAmerican journal of translational research · 2021
    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

7 authors at 3 institutions in 1 country.

Zi-Yuan Nie *Department of Hematology, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000 China.
Ming-Hui Zhao *Department of Radiology, Affiliated Hospital of Hebei University, Baoding, 071000 China.
Bao-Qian ChengDepartment of Clinical Medicine, Hebei Medical University, Shijiazhuang, 050000 China.
Rong-Fang PanDepartment of Nutrition, The Affiliated Hospital of Qingdao University, Qingdao, 266003 China.
Tian-Rui WangDepartment of Orthopaedic Surgery, The Third Hospital of Hebei Medical University, Shijiazhuang, 050051 China.
Yan QinCentral Laboratory, Affiliated Hospital of Hebei University, 212 Yuhua East Road, Baoding, 071000 China.ORCID 0000-0002-8811-7187
Xue-Jun ZhangDepartment of Hematology, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000 China.
Hebei Medical University · CNAffiliated Hospital of Hebei University · CNQingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe roots of

methodsCCK-8 assays and BrdU stain were used to evaluate cell proliferation ability. Western blot analysis was used to detect protein expression. miR-497-5p expression level was detected by using qRT-PCR, and Annexin V-FITC/propidium iodide (PI) was used to detect cell apoptosis.

resultsHere we reported that Tan IIA could inhibit cell proliferation, induce cell cycle arrest, and promote cell apoptosis in acute myeloid leukemia (AML) cells. Thus, Tan IIA had the anti-cancer activity in AML cell lines, which was likely mediated by up-regulation of miR-497-5p expression. Our data further showed that in AML cells, the same effects were observed with overexpression of miR-497-5p by a miR-497-5p mimic. We demonstrated that Tan IIA could inhibit the expression of AKT3 by up-regulating the expression of miR-497-5p. We subsequently identified that AKT3 was the direct target of miR-497-5p, and that treatment with Tan IIA obviously reversed the effect of treatment with an miR-497-5p inhibitor under harsh conditions. In turn, PCNA expression was increased and cleaved Caspase-3 was suppressed, which contributed to the growth of AML cells.

conclusionsOur results showed that Tan IIA could inhibit cell proliferation in AML cells through miR-497-5p-mediated AKT3 downregulation pathway.

Indexed as

Acute myeloid leukemiaAKT3ApoptosismiR-497-5pProliferationTanshinone IIA

Identifiers

PMID32782437
PMCPMC7412841
OpenAlexW3047913553

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.