MicroRNA-203a-3p may prevent the development of thyroid papillary carcinoma via repressing MAP3K1 and activating autophagy.
J Clin Lab Anal
; 36(6): e24470, 2022 Jun.
Article
en En
| MEDLINE
| ID: mdl-35524422
ABSTRACT
BACKGROUND:
Papillary thyroid carcinoma (PTC) grows slowly but has a great risk of metastasis. MicroRNAs are well known as vital tumor-related gene regulators. In PTC, the role of miR-203a-3p and the underlying mechanisms remain not completely understood.METHODS:
We conducted CCK8 assay, wound healing assay, transwell experiment and flow cytometry analyses to investigate the function of miRNA-203a-3p. The interaction of miRNA-203a-3p with its gene MAP3K1 was characterized by quantitative real-time polymerase chain reaction, western blotting and luciferase assay.RESULTS:
We found that the levels of miRNA-203a-3p were statistically decreased in PTC tissues. When mimics were delivered to TPC-1 and KTC-1 cells to upregulate miR-203a-3p, it was observed that cell proliferation, metastatic abilities and cell cycle process were prevented but cell apoptosis was enhanced. Furthermore, we proved the interaction between MAP3K1 and miR-203a-3p. Intriguingly, similar to miR-203a-3p mimics, siMAP3K1 showed a tumor-suppressive effect, and this effect could be reversed when miR-203a-3p was simultaneously inhibited. Finally, selected autophagy-linked proteins such as LC3 Beclin-1 were detected and found to be increased when miR-203a-3p was upregulated or MAP3K1 was inhibited.CONCLUSION:
Overall, miR-203a-3p inhibits the oncogenic characteristics of TPC-1 and KTC-1 cells via suppressing MAP3K1 and activating autophagy. Our findings might enrich the understanding and the therapeutic strategies of PTC.Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Neoplasias de la Tiroides
/
Carcinoma Papilar
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MicroARNs
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Quinasa 1 de Quinasa de Quinasa MAP
Límite:
Humans
Idioma:
En
Revista:
J Clin Lab Anal
Asunto de la revista:
TECNICAS E PROCEDIMENTOS DE LABORATORIO
Año:
2022
Tipo del documento:
Article
País de afiliación:
China