Evidence map›Paper›PMID 26319392›Full record

ArticleJournal of cancer research and clinical oncology2016

Amplified HMGA2 promotes cell growth by regulating Akt pathway in AML.

Li Tan, Xiaoping Wei, Lixia Zheng, Jincai Zeng, Haibo Liu, Shaojiang Yang, Huo Tan

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

45 citing papers in PubMed, 73 citations in OpenAlex.

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  10. Complete miRNA-15/16 loss in mice promotes hematopoietic progenitor expansion and a myeloid-biased hyperproliferative state.Proceedings of the National Academy of Sciences of the United States of America · 2023
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  17. Observational
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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.

Li TanCenter of Oncology and Hematology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510230, China. tanya_tanli@163.com.
Xiaoping WeiClinical Laboratory, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120, China.
Lixia ZhengCenter of Oncology and Hematology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510230, China.
Jincai ZengCenter of Oncology and Hematology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510230, China.
Haibo LiuKey Laboratory for Major Obstetric Diseases of Guangdong Province, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510150, China.
Shaojiang YangCenter of Oncology and Hematology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510230, China.
Huo TanCenter of Oncology and Hematology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510230, China.
Guangzhou Medical University · CNFirst Affiliated Hospital of Guangzhou Medical University · CNThird Affiliated Hospital of Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe aim of this study was to investigate how the amplification of HMGA2 contributes to acute myeloid leukemia (AML) cell proliferation.

methodsThe amplification and expression of HMGA2 were examined by FISH, qRT-PCR and Western blot in AML cases. The effect of HMGA2 knockdown on cell proliferation was analyzed with XTT, colony-forming assays and BrdUrd incorporation assays. The effects of HMGA2 knockdown on cell cycle were studied by flow cytometry analysis. The progression of AML cells in vivo was examined by the xenografted tumor model. The interaction between Akt pathway and HMGA2 was examined by Western blot.

resultsHMGA2 is amplified in AML, and the levels of HMGA2 messenger RNA (mRNA) and protein expressed in AML cells were significantly higher than those in normal cells, which may be related to NR and prognosis of AML patients. Reduction in HMGA2 expression in AML cells inhibited cell proliferation through a decrease in the protein expression of pAkt and pmTOR, compared with control cells.

conclusionsHMGA2 is predominantly amplified and expressed in AML cells, and that aberrant expression of HMGA2 induces AML cell proliferation through the PI3K/Akt/mTOR signaling pathway. Inhibition of HMGA2 expression represents an attractive target for AML therapy.

Indexed as

AdolescentAdultAgedAnimalsCell Growth ProcessesCell Line, TumorGene AmplificationGene Knockdown TechniquesHeterograftsHL-60 CellsHMGA2 ProteinHumansIn Situ Hybridization, FluorescenceLeukemia, Myeloid, AcuteMaleMiceHMGA2 ProteinMTOR protein, humanProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAkt pathwayAMLHMGA2Proliferation

Identifiers

PMID26319392
PMCPMC11819090
OpenAlexW1154501214

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.