Bromodomain-containing protein 4 regulates interleukin-34 expression in mouse ovarian cancer cells.

Bromodomain-containing protein 4 Cytokine induction Gene regulation Interleukin-34 JQ1 Tumor cell biology Tumor promotor

Journal

Inflammation and regeneration
ISSN: 1880-9693
Titre abrégé: Inflamm Regen
Pays: England
ID NLM: 101479577

Informations de publication

Date de publication:
2020
Historique:
received: 05 11 2019
accepted: 30 06 2020
entrez: 19 10 2020
pubmed: 20 10 2020
medline: 20 10 2020
Statut: epublish

Résumé

Interleukin (IL)-34 acts as an alternative ligand for the colony-stimulating factor-1 receptor and controls the biology of myeloid cells, including survival, proliferation, and differentiation. IL-34 has been reported to be expressed in cancer cells and to promote tumor progression and metastasis of certain cancers via the promotion of angiogenesis and immunosuppressive macrophage differentiation. We have shown in our previous reports that targeting IL-34 in chemo-resistant tumors in vitro resulted in a remarkable inhibition of tumor growth. Also, we reported poor prognosis in patients with IL-34-expressing tumor. Therefore, blocking of IL-34 is considered as a promising therapeutic strategy to suppress tumor progression. However, the molecular mechanisms that control IL-34 production are still largely unknown. IL-34 producing ovarian cancer cell line HM-1 was treated by bromodomain and extra terminal inhibitor JQ1. The mRNA and protein expression of IL-34 was evaluated after JQ1 treatment. Chromatin immunoprecipitation was performed to confirm the involvement of bromodomain-containing protein 4 (Brd4) in the regulation of the We identified Brd4 as one of the critical molecules that regulate The results unveiled for the first time the responsible molecule Brd4 that regulates

Sections du résumé

BACKGROUND BACKGROUND
Interleukin (IL)-34 acts as an alternative ligand for the colony-stimulating factor-1 receptor and controls the biology of myeloid cells, including survival, proliferation, and differentiation. IL-34 has been reported to be expressed in cancer cells and to promote tumor progression and metastasis of certain cancers via the promotion of angiogenesis and immunosuppressive macrophage differentiation. We have shown in our previous reports that targeting IL-34 in chemo-resistant tumors in vitro resulted in a remarkable inhibition of tumor growth. Also, we reported poor prognosis in patients with IL-34-expressing tumor. Therefore, blocking of IL-34 is considered as a promising therapeutic strategy to suppress tumor progression. However, the molecular mechanisms that control IL-34 production are still largely unknown.
METHODS METHODS
IL-34 producing ovarian cancer cell line HM-1 was treated by bromodomain and extra terminal inhibitor JQ1. The mRNA and protein expression of IL-34 was evaluated after JQ1 treatment. Chromatin immunoprecipitation was performed to confirm the involvement of bromodomain-containing protein 4 (Brd4) in the regulation of the
RESULTS RESULTS
We identified Brd4 as one of the critical molecules that regulate
CONCLUSION CONCLUSIONS
The results unveiled for the first time the responsible molecule Brd4 that regulates

Identifiants

pubmed: 33072227
doi: 10.1186/s41232-020-00129-4
pii: 129
pmc: PMC7556959
doi:

Types de publication

Journal Article

Langues

eng

Pagination

25

Informations de copyright

© The Author(s) 2020.

Déclaration de conflit d'intérêts

Competing interestsThe authors declare that they have no competing interests.

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Auteurs

Nanumi Han (N)

Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University, Kita-15 Nishi-7, Kita-ku, Sapporo, Hokkaido 060-0815 Japan.

Delnur Anwar (D)

Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University, Kita-15 Nishi-7, Kita-ku, Sapporo, Hokkaido 060-0815 Japan.

Naoki Hama (N)

Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University, Kita-15 Nishi-7, Kita-ku, Sapporo, Hokkaido 060-0815 Japan.

Takuto Kobayashi (T)

Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University, Kita-15 Nishi-7, Kita-ku, Sapporo, Hokkaido 060-0815 Japan.

Hidefumi Suzuki (H)

Department of Molecular Biology, School of Medicine, Yokohama City University, 3-9 of Fukuura Kanazawa-ku, Yokohama, Kanagawa 236-0004 Japan.

Hidehisa Takahashi (H)

Department of Molecular Biology, School of Medicine, Yokohama City University, 3-9 of Fukuura Kanazawa-ku, Yokohama, Kanagawa 236-0004 Japan.

Haruka Wada (H)

Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University, Kita-15 Nishi-7, Kita-ku, Sapporo, Hokkaido 060-0815 Japan.

Ryo Otsuka (R)

Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University, Kita-15 Nishi-7, Kita-ku, Sapporo, Hokkaido 060-0815 Japan.

Muhammad Baghdadi (M)

Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University, Kita-15 Nishi-7, Kita-ku, Sapporo, Hokkaido 060-0815 Japan.

Ken-Ichiro Seino (KI)

Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University, Kita-15 Nishi-7, Kita-ku, Sapporo, Hokkaido 060-0815 Japan.

Classifications MeSH