Evidence map›Paper›PMID 33603066›Full record

ArticleScientific reports2021

Overexpression of aberrant Wnt5a and its effect on acquisition of malignant phenotypes in adult T-cell leukemia/lymphoma (ATL) cells.

Kazumi Nakano, Yohei Chihara, Seiichiro Kobayashi, Masako Iwanaga, Atae Utsunomiya, Toshiki Watanabe, Kaoru Uchimaru

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 38% 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

9 citing papers in PubMed, 9 citations in OpenAlex.

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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 5 institutions in 1 country.

Kazumi NakanoDepartment of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, 4-6-1, Shirokanedai, Minatoku, Tokyo, 108-8639, Japan. nakanokz@edu.k.u-tokyo.ac.jp.
Yohei ChiharaDepartment of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, 4-6-1, Shirokanedai, Minatoku, Tokyo, 108-8639, Japan.
Seiichiro KobayashiDepartment of Hematology, Kanto Rosai Hospital, Kanagawa, Japan.
Masako IwanagaDepartment of Clinical Epidemiology, Graduate School of Biomedical Science, Nagasaki University, Nagasaki, Japan.
Atae UtsunomiyaDepartment of Hematology, Imamura General Hospital, Kagoshima, Japan.
Toshiki WatanabeLaboratory of Practical Management of Medical Information, Graduate School of Medicine, St. Marianna University, Kanagawa, Japan.
Kaoru UchimaruDepartment of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, 4-6-1, Shirokanedai, Minatoku, Tokyo, 108-8639, Japan.
The University of Tokyo · JPImamura Hospital · JPNagasaki University · JPSt. Marianna University School of Medicine · JPYokohama Rosai Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Wnt5a is a ligand of the non-canonical Wnt signaling pathway involved in cell differentiation, motility, and inflammatory response. Adult T-cell leukemia/lymphoma (ATL) is one of the most aggressive T-cell malignancies caused by infection of human T-cell leukemia virus type1 (HTLV-1). Among subtypes of ATL, acute-type ATL cells are particularly resistant to current multidrug chemotherapies and show remarkably high cell-proliferative and invasive phenotypes. Here we show a dramatic increase of WNT5A gene expression in acute-type ATL cells compared with those of indolent-type ATL cells. Treatment with IWP-2 or Wnt5a-specific knockdown significantly suppressed cell growth of ATL-derived T-cell lines. We demonstrated that the overexpression of c-Myb and FoxM1 was responsible for the synergistic activation of the WNT5A promoter. Also, a WNT5A transcript variant without the exon4 (the ΔE4-WNT5A mRNA), encoding ΔC-Wnt5 (1-136aa of 380aa), is overexpressed in acute-type ATL cells. The ΔC-Wnt5a is secreted extracellularly and enhances cellular migration/invasion to a greater extent compared with wildtype (WT)-Wnt5a. Moreover, the ΔC-Wnt5a secretion was not suppressed by IWP-2, indicating that this mutant Wnt5a is secreted via a different pathway from the WT-Wnt5a. Taken together, synergistic overexpression of the ΔC-Wnt5a by c-Myb and FoxM1 may be responsible for the malignant phenotype of acute-type ATL cells.

Indexed as

Cell DifferentiationCell Line, TumorCell MovementCell ProliferationDeltaretrovirusGene ExpressionHumansJurkat CellsLeukemia-Lymphoma, Adult T-CellPhenotypeT-LymphocytesWnt-5a ProteinWnt Signaling PathwayWnt-5a ProteinWNT5A protein, human

Identifiers

PMID33603066
PMCPMC7892546
OpenAlexW3130898880

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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.