The role of circRNA polyribonucleotide nucleoside transferase 1 on Gestational Diabetes Mellitus.


Journal

Cellular and molecular biology (Noisy-le-Grand, France)
ISSN: 1165-158X
Titre abrégé: Cell Mol Biol (Noisy-le-grand)
Pays: France
ID NLM: 9216789

Informations de publication

Date de publication:
30 Jun 2022
Historique:
received: 04 07 2022
entrez: 13 10 2022
pubmed: 14 10 2022
medline: 18 10 2022
Statut: epublish

Résumé

This study aimed to focus on the mechanism of circRNA polyribonucleotide nucleoside transferase 1 (circ-PNPT1)-mediated miR-889-3p/PAK1 on gestational diabetes mellitus (GDM). Placental tissues from normal pregnancy and GDM patients were collected to detect the levels of circ-PNPT1, miR-889-3p, and PAK1. The high glucose-induced human trophoblast cells HTR-8/SVneo were adopted to stimulate the GDM model in vitro (HG group) and were transfected with lentivirus to silence circ-PNPT1 (si-circ-PNPT1 group) and mimic to overexpress miR-889-3p (miR-889-3p group). Cell proliferation, apoptosis, migration, and invasion were detected by CKK-8, flow cytometry, Transwell, and scratch assay, respectively. The results showed that the expressions of circ-PNPT1 and PAK1 in the GDM patients were up-regulated, and miR-889-3p was down-regulated (P< 0.05). Compared with cells in the control group, the circ-PNPT1 and PAK1 in the HG group were up-regulated, and miR-889-3p was down-regulated (P< 0.05). The cell proliferation, migration, and invasion abilities were weakened, and the apoptosis rate increased (P< 0.05). E-cadherin protein was elevated, and the N-cadherin and Vimentin decreased (P< 0.05). Compared with the HG group, the expressions of circ-PNPT1 and PAK1 in the other two groups decreased, and miR-889-3p increased (P< 0.05). The cell proliferation, migration, and invasion were enhanced, and the apoptosis rate decreased (P< 0.05). E-cadherin, N-cadherin, and Vimentin decreased (P< 0.05). There were targeted binding sites for miR-889-3p with circ-PNPT1 and PAK1, indicating circ-PNPT1 promoted HG-induced trophoblast dysfunction through the miR-889-3p/PAK1 axis.

Identifiants

pubmed: 36227662
doi: 10.14715/cmb/2022.68.6.24
doi:

Substances chimiques

Cadherins 0
MicroRNAs 0
Mitochondrial Proteins 0
Nucleosides 0
Polyribonucleotides 0
RNA, Circular 0
Vimentin 0
Transferases EC 2.-
Exoribonucleases EC 3.1.-
PNPT1 protein, human EC 3.1.13.-
Glucose IY9XDZ35W2

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

148-154

Auteurs

Xiaolu Chen (X)

Department of Obstetrics and Gynecology, Taizhou First People's Hospital, Taizhou 318020, Zhejiang Province, China. chenxiaolu2022@yandex.com.

Jiaou Huang (J)

Department of Obstetrics and Gynecology, Taizhou First People's Hospital, Taizhou 318020, Zhejiang Province, China. chenxiaolu2022@yandex.com.

Yangying Peng (Y)

Department of Obstetrics and Gynecology, Taizhou First People's Hospital, Taizhou 318020, Zhejiang Province, China. chenxiaolu2022@yandex.com.

Yu Han (Y)

Department of Obstetrics and Gynecology, Taizhou First People's Hospital, Taizhou 318020, Zhejiang Province, China. chenxiaolu2022@yandex.com.

Xiaoyan Wang (X)

Department of Obstetrics and Gynecology, Taizhou First People's Hospital, Taizhou 318020, Zhejiang Province, China. chenxiaolu2022@yandex.com.

Chuanfa Tu (C)

Department of Endocrinology and Metabolism, Taizhou First People's Hospital, Taizhou 318020, Zhejiang Province, China. chenxiaolu2022@yandex.com.

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Classifications MeSH