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1.
J Biol Regul Homeost Agents ; 34(5): 1709-1717, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33176419

RESUMO

Preeclampsia (PE) may induce gestational failure, threatening a significant number of pregnant women. Recently, microRNAs (miRNAs) have been reported to participate in PE progression, whereas the precise functions and potential mechanisms of miR-20b in placental trophoblast cells as well as in PE progression remain poorly understood. In the present study, real-time quantitative polymerase chain reaction (RT-qPCR) analysis was used to detect expressions of miR-20b and myeloid cell leukemin- 1(MCL-1) mRNA. Cell viability was investigated by cell counting kit-8(CCK-8) assays. Cell invasion and migration abilities were determined by Transwell assays. Western blot was performed to detect MCL-1 protein expressions. The interaction between miR-20b and MCL-1 was investigated by bioinformatics analysis and luciferase activity assay. The results of the study demonstrated that miR-20b was highly expressed in placental tissues of patients with PE. Moreover, miR-20b overexpression inhibited HTR8/ SVneo cell proliferation, invasion and migration. Furthermore, MCL-1 was targeted by miR-20b, and MCL-1 restoration could partially attenuate the effect of miR-20b on HTR8/SVneo cells. In conclusion, the results indicate that miR-20b may contribute to PE through inhibiting proliferation, invasion and migration of placental trophoblast cells by targeting MCL-1. Therefore, miR-20b may be used as a notable biomarker for the diagnosis, prevention, and treatment of PE. MiR-20b targeting MCL-1 deserves further investigation in order to explore their potential role in PE.


Assuntos
MicroRNAs/genética , Pré-Eclâmpsia , Feminino , Humanos , Proteína de Sequência 1 de Leucemia de Células Mieloides , Pré-Eclâmpsia/genética , Gravidez , Trofoblastos
2.
J Biol Regul Homeost Agents ; 34(2)2020 Apr 24.
Artigo em Inglês | MEDLINE | ID: mdl-32329296

RESUMO

Recently, important regulatory mechanisms of microRNAs (miRNAs) have been widely reported in human cancers including cervical cancer. The purpose of this study is to preliminarily clarify the function of miR-1294 in cervical cancer. The expression of miR-1294 or FLOT1 was detected using RT-qPCR or Western blot analysis. MTT, Transwell and luciferase reporter assays were used to explore the functional mechanism of miR-1294. The results showed that miR-1294 expression was decreased in cervical cancer. Functionally, overexpression of miR-1294 restrained the viability and metastasis of cervical cancer cells. MiR-1294 can also block EMT and suppress ß-catenin expression in cervical cancer cells. Additionally, FLOT1 was confirmed to be a direct target of miR-1294. The knockdown of FLOT1 impeded the progression of cervical cancer. More importantly, miR-1294 inhibited the occurrence of cervical cancer by interacting with FLOT1. In conclusion, miR-1294 inhibits cell viability, migration and invasion by suppressing FLOT1 expression.

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