MiR-29b may suppresses peritoneal metastases through inhibition of the mesothelial-mesenchymal transition (MMT) of human peritoneal mesothelial cells.


Journal

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

Informations de publication

Date de publication:
07 01 2022
Historique:
received: 02 08 2021
accepted: 30 11 2021
entrez: 8 1 2022
pubmed: 9 1 2022
medline: 24 2 2022
Statut: epublish

Résumé

Peritoneal dissemination is a major metastatic pathway for gastrointestinal and ovarian malignancies. The miR-29b family is downregulated in peritoneal fluids in patients with peritoneal metastases (PM). We examined the effect of miR-29b on mesothelial cells (MC) which play critical a role in the development of PM through mesothelial-mesenchymal transition (MMT). Human peritoneal mesothelial cells (HPMCs) were isolated from surgically resected omental tissue and MMT induced by stimulation with 10 ng/ml TGF-β1. MiR-29b mimics and negative control miR were transfected by lipofection using RNAiMAX and the effects on the MMT evaluated in vitro. HPMC produced substantial amounts of miR-29b which was markedly inhibited by TGF-β1. TGF-β1 stimulation of HPMC induced morphological changes with decreased expression of E-cadherin and calretinin, and increased expression of vimentin and fibronectin. TGF-β1 also enhanced proliferation and migration of HPMC as well as adhesion of tumor cells in a fibronectin dependent manner. However, all events were strongly abrogated by simultaneous transfection of miR-29b. MiR-29b inhibits TGF-β1 induced MMT and replacement of miR-29b in the peritoneal cavity might be effective to prevent development of PM partly through the effects on MC.

Identifiants

pubmed: 34997082
doi: 10.1038/s41598-021-04065-2
pii: 10.1038/s41598-021-04065-2
pmc: PMC8742040
doi:

Substances chimiques

Antigens, CD 0
CALB2 protein, human 0
CDH1 protein, human 0
Cadherins 0
Calbindin 2 0
Fibronectins 0
MIRN29B1 microRNA, human 0
MicroRNAs 0
Transforming Growth Factor beta1 0
VIM protein, human 0
Vimentin 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

205

Subventions

Organisme : Japan Society for the Promotion of Science
ID : 20K07704

Informations de copyright

© 2022. The Author(s).

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Auteurs

Yuki Kimura (Y)

Department of Surgery, Jichi Medical University, Shimotsuke, Tochigi, Japan.

Hideyuki Ohzawa (H)

Department of Clinical Oncology, Jichi Medical University, Shimotsuke, Tochigi, Japan.

Hideyo Miyato (H)

Department of Surgery, Jichi Medical University, Shimotsuke, Tochigi, Japan.

Yuki Kaneko (Y)

Department of Surgery, Jichi Medical University, Shimotsuke, Tochigi, Japan.

Akira Saito (A)

Department of Surgery, Jichi Medical University, Shimotsuke, Tochigi, Japan.

Kazuya Takahashi (K)

Department of Surgery, Jichi Medical University, Shimotsuke, Tochigi, Japan.

Mineyuki Tojo (M)

Department of Surgery, Jichi Medical University, Shimotsuke, Tochigi, Japan.

Hironori Yamaguchi (H)

Department of Clinical Oncology, Jichi Medical University, Shimotsuke, Tochigi, Japan.

Kentaro Kurashina (K)

Department of Surgery, Jichi Medical University, Shimotsuke, Tochigi, Japan.

Shin Saito (S)

Department of Surgery, Jichi Medical University, Shimotsuke, Tochigi, Japan.

Yoshinori Hosoya (Y)

Department of Surgery, Jichi Medical University, Shimotsuke, Tochigi, Japan.

Alan Kawarai Lefor (AK)

Department of Surgery, Jichi Medical University, Shimotsuke, Tochigi, Japan.

Naohiro Sata (N)

Department of Surgery, Jichi Medical University, Shimotsuke, Tochigi, Japan.

Joji Kitayama (J)

Department of Surgery, Jichi Medical University, Shimotsuke, Tochigi, Japan. kitayama@jichi.ac.jp.
Center for Clinical Research, Jichi Medical University Hospital, Shimotsuke, Tochigi, Japan. kitayama@jichi.ac.jp.

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Classifications MeSH