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


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
18 02 2021
Historique:
received: 04 08 2020
accepted: 03 02 2021
entrez: 19 2 2021
pubmed: 20 2 2021
medline: 15 12 2021
Statut: epublish

Résumé

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.

Identifiants

pubmed: 33603066
doi: 10.1038/s41598-021-83613-2
pii: 10.1038/s41598-021-83613-2
pmc: PMC7892546
doi:

Substances chimiques

WNT5A protein, human 0
Wnt-5a Protein 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

4114

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Auteurs

Kazumi Nakano (K)

Department 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 Chihara (Y)

Department 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 Kobayashi (S)

Department of Hematology, Kanto Rosai Hospital, Kanagawa, Japan.

Masako Iwanaga (M)

Department of Clinical Epidemiology, Graduate School of Biomedical Science, Nagasaki University, Nagasaki, Japan.

Atae Utsunomiya (A)

Department of Hematology, Imamura General Hospital, Kagoshima, Japan.

Toshiki Watanabe (T)

Laboratory of Practical Management of Medical Information, Graduate School of Medicine, St. Marianna University, Kanagawa, Japan.

Kaoru Uchimaru (K)

Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, 4-6-1, Shirokanedai, Minatoku, Tokyo, 108-8639, Japan.

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