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miR-21 Is Overexpressed in Hydatidiform Mole Tissues and Promotes Proliferation, Migration, and Invasion in Choriocarcinoma Cells
- Source :
- International Journal of Gynecologic Cancer. 27:364-374
- Publication Year :
- 2017
- Publisher :
- BMJ, 2017.
-
Abstract
- ObjectiveThe aims of this study were to make clear whether miR-21 was dysregulated in hydatidiform mole (HM) tissues and choriocarcinoma (CCA) cells, to elucidate whether aberrant miR-21 expression would affect the function of CCA cells, and to find out whether there was a relationship between miR-21 andAKT,PDCD4, andPTENin CCA cells.MethodsFresh and formalin-fixed, paraffin-embedded trophoblastic tissues (normal first trimester placentas and HMs) were retrieved from the biobank in the International Peace Maternity and Child Health Hospital, Shanghai Jiao Tong University. Choriocarcinoma JAR and JEG-3 cells were cultured. Expression of miR-21 in trophoblast cells and tissues was examined by quantitative real-time polymerase chain reaction. Location and distribution of miR-21 in trophoblast tissues were determinated by in situ hybridization and fluorescent in situ hybridization. The effect of miR-21 on JAR and JEG-3 cells was tested by miR-21 mimics and inhibitor transfection, followed by cell viability assay, flow cytometric analysis, and Transwell analysis. Interaction between miR-21 and its target genes in CCA cells was verified by quantitative real-time polymerase chain reaction, Western blot, and luciferase report system.ResultsWe originally found miR-21 was markedly upregulated in HM tissues compared with normal first trimester placentas. The expression of miR-21 was exclusively confined in trophoblastic layers. Furthermore, we discovered miR-21 was significantly increased in JAR and JEG-3 cells compared with normal primary human trophoblastic cells. Moreover, we demonstrated miR-21 could promote proliferation, migration, and invasion of CCA cells. We furthermore proved miR-21 negatively regulated PDCD4 and PTEN in CCA cells and targeted toPDCD43′UTR directly. In addition, we confirmed that miR-21 could activate Akt pathway by phosphorylating Akt at Ser 473.ConclusionsOur results suggested miR-21 was responsible for aggressive phenotype of gestational trophoblastic disease and had the potential diagnostic and therapeutic values for gestational trophoblastic neoplasm.
- Subjects :
- 0301 basic medicine
Transfection
03 medical and health sciences
0302 clinical medicine
Biomimetic Materials
Cell Movement
Pregnancy
Cell Line, Tumor
medicine
Trophoblastic neoplasm
Humans
PTEN
Neoplasm Invasiveness
Choriocarcinoma
Viability assay
Phosphorylation
In Situ Hybridization
In Situ Hybridization, Fluorescence
PI3K/AKT/mTOR pathway
Cell Proliferation
biology
business.industry
Gestational trophoblastic disease
PTEN Phosphohydrolase
RNA-Binding Proteins
Obstetrics and Gynecology
Trophoblast
Hydatidiform Mole
medicine.disease
Up-Regulation
MicroRNAs
030104 developmental biology
medicine.anatomical_structure
Oncology
030220 oncology & carcinogenesis
Uterine Neoplasms
embryonic structures
biology.protein
Cancer research
Female
Apoptosis Regulatory Proteins
business
Proto-Oncogene Proteins c-akt
Subjects
Details
- ISSN :
- 15251438 and 1048891X
- Volume :
- 27
- Database :
- OpenAIRE
- Journal :
- International Journal of Gynecologic Cancer
- Accession number :
- edsair.doi.dedup.....86b41f6801287907414bccbeb0dfcdae