Overexpression of miR-199/214 is a distinctive feature of iron-induced and asbestos-induced sarcomatoid mesothelioma in rats.


Journal

Cancer science
ISSN: 1349-7006
Titre abrégé: Cancer Sci
Pays: England
ID NLM: 101168776

Informations de publication

Date de publication:
Jun 2020
Historique:
received: 03 12 2019
revised: 17 03 2020
accepted: 24 03 2020
pubmed: 6 4 2020
medline: 20 6 2020
entrez: 6 4 2020
Statut: ppublish

Résumé

Malignant mesothelioma (MM) is one of the most lethal tumors in humans. The onset of MM is linked to exposure to asbestos, which generates reactive oxygen species (ROS). ROS are believed to be derived from the frustrated phagocytosis and the iron in asbestos. To explore the pathogenesis of MM, peritoneal MM was induced in rats by the repeated intraperitoneal injection of iron saccharate and nitrilotriacetate. In the present study, we used microarray techniques to screen the microRNA (miR) expression profiles of these MM. We observed that the histological subtype impacted the hierarchical clustering of miR expression profiles and determined that miR-199/214 is a distinctive feature of iron saccharate-induced sarcomatoid mesothelioma (SM). Twist1, a transcriptional regulator of the epithelial-mesenchymal transition, has been shown to activate miR-199/214 transcription; thus, the expression level of Twist1 was examined in iron-induced and asbestos-induced mesotheliomas in rats. Twist1 was exclusively expressed in iron saccharate-induced SM but not in the epithelioid subtype. The Twist1-miR-199/214 axis is activated in iron saccharate-induced and asbestos-induced SM. The expression levels of miR-214 and Twist1 were correlated in an asbestos-induced MM cell line, suggesting that the Twist1-miR-199/214 axis is preserved. MeT5A, an immortalized human mesothelial cell line, was used for the functional analysis of miR. The overexpression of miR-199/214 promoted cellular proliferation, mobility and phosphorylation of Akt and ERK in MeT5A cells. These results indicate that miR-199/214 may affect the aggressive biological behavior of SM.

Identifiants

pubmed: 32248600
doi: 10.1111/cas.14405
pmc: PMC7293088
doi:

Substances chimiques

MIRN199 microRNA, rat 0
MIRN214 microRNA, human 0
MicroRNAs 0
Mirn214 microRNA, rat 0
Twist-Related Protein 1 0
mirn199 microRNA, human 0
Asbestos 1332-21-4
Iron E1UOL152H7

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2016-2027

Subventions

Organisme : Ministry of Education, Culture, Sports, Science and Technology
Organisme : Japan Society for the Promotion of Science
ID : Young Scientist (B)(23790440)
Organisme : Japan Society for the Promotion of Science
ID : Young Scientist (B)(25860292)
Organisme : JSPS Kakenhi
ID : JP17H04064
Organisme : JSPS Kakenhi
ID : JP19H05462
Organisme : JST CREST
ID : JPMJCR19H4

Informations de copyright

© 2020 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.

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Auteurs

Yasumasa Okazaki (Y)

Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Shan Hwu Chew (SH)

Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Hirotaka Nagai (H)

Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Yoriko Yamashita (Y)

Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Hiroki Ohara (H)

Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Li Jiang (L)

Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Shinya Akatsuka (S)

Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Takashi Takahashi (T)

Division of Molecular Carcinogenesis, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Aichi Cancer Center Research Institute, Nagoya, Japan.

Shinya Toyokuni (S)

Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, Japan.

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