Long non-coding RNA PCAT-1 promotes tumor progression by inhibiting miR-129-5p in human ovarian cancer
Introduction Ovarian cancer (OC) is one of the most common malignancies and the leading cause of cancer-related death among women. The long non-coding RNA Prostate cancer-associated transcript-1 (PCAT-1) has been reported to play important roles in multiple human cancers. However, the role of PCAT-1...
Guardado en:
| Autores principales: | , , , , , , |
|---|---|
| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
Termedia Publishing House
2019
|
| Materias: | |
| Acceso en línea: | https://doaj.org/article/93e84879755a4c8cb31994c603c07f33 |
| Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
| Sumario: | Introduction
Ovarian cancer (OC) is one of the most common malignancies and the leading cause of cancer-related death among women. The long non-coding RNA Prostate cancer-associated transcript-1 (PCAT-1) has been reported to play important roles in multiple human cancers. However, the role of PCAT-1 in OC has never been investigated. The purpose of this study was to investigate the expression and roles of PCAT-1 in OC.
Material and methods
Expression of PCAT-1 and miR-129-5p in OC tissues and cell lines was determined by qRT-PCR. Cell proliferation and apoptosis were analyzed by MTT assay and flow cytometry, respectively. The interaction between PCAT-1 and miR-129-5p was demonstrated by luciferase reporter assay.
Results
PCAT-1 is significantly upregulated in OC tissues and cell lines (p < 0.05). Overexpression of PCAT-1 promotes proliferation of OC cells and inhibits their apoptosis (p < 0.05). In addition, miR-129-5p is markedly downregulated in OC and its level is inversely correlated with PCAT-1 expression in OC tumor tissues (p < 0.05). miR-129-5p inhibits proliferation and induces apoptosis in OC cell lines (p < 0.05). Furthermore, it has been demonstrated that miR-129-5p is directly targeted by PCAT-1 and miR-129-5p overexpression can effectively attenuate the effects of PCAT-1 on the proliferation and apoptosis of OC cells.
Conclusions
Our results suggest that PCAT-1 functions as an oncogene by inhibiting miR-129-5p in OC and silencing PCAT-1 may be a novel therapeutic strategy in the treatment of OC. |
|---|