scholarly journals Long Non-coding RNA LOC285194 Promotes Epithelial Ovarian Cancer Progression via the Apoptosis Signaling Pathway

In Vivo ◽  
2021 ◽  
Vol 36 (1) ◽  
pp. 121-131
Author(s):  
GA WON YIM ◽  
DAE WOO LEE ◽  
JAE IN KIM ◽  
YOUNG TAE KIM
2021 ◽  
Vol 12 (6) ◽  
pp. 1660-1668
Author(s):  
Yinglei Liu ◽  
Boqun Xu ◽  
Manhua Liu ◽  
Haifeng Qiao ◽  
Siming Zhang ◽  
...  

2016 ◽  
Vol 12 (2) ◽  
pp. 1361-1366 ◽  
Author(s):  
Qingjuan Chen ◽  
Yongyong Su ◽  
Xiaopeng He ◽  
Weian Zhao ◽  
Caixia Wu ◽  
...  

2017 ◽  
Vol 359 (1) ◽  
pp. 185-194 ◽  
Author(s):  
Yuan Cao ◽  
Huirong Shi ◽  
Fang Ren ◽  
Yanyan Jia ◽  
Ruitao Zhang

2020 ◽  
Author(s):  
Juanjuan Shi ◽  
Xijian Xu ◽  
Dan Zhang ◽  
Jiuyan Zhang ◽  
Hui Yang ◽  
...  

Abstract Background: Long non-coding RNA PTPRG antisense RNA 1 (PTPRG-AS1) deregulation has been reported in various human malignancies and identified as an important modulator of cancer development. Few reports have focused on the detailed role of PTPRG-AS1 in epithelial ovarian cancer (EOC) and its underlying mechanism. This study aimed to determine the physiological function of PTPRG-AS1 in EOC. A series of experiments were also performed to identify the mechanisms through which PTPRG-AS1 exerts its function in EOC.Methods: Reverse transcription-quantitative polymerase chain reaction was used to determine PTPRG-AS1 expression in EOC tissues and cell lines. PTPRG-AS1 was silenced in EOC cells and studied with respect to cell proliferation, apoptosis, migration, and invasion in vitro and tumor growth in vivo. The putative miRNAs that target PTPRG-AS1 were predicted using bioinformatics analysis and further confirmed in luciferase reporter and RNA immunoprecipitation assays.Results: Our data verified the upregulation of PTPRG-AS1 in EOC tissues and cell lines. High PTPRG-AS1 expression was associated with shorter overall survival in patients with EOC. Functionally, EOC cell proliferation, migration, invasion in vitro, and tumor growth in vivo were suppressed by PTPRG-AS1 silencing. In contrast, cell apoptosis was promoted by loss of PTPRG-AS1. Regarding the mechanism, PTPRG-AS1 could serve as a competing endogenous RNA in EOC cells by decoying microRNA-545-3p (miR-545-3p), thereby elevating histone deacetylase 4 (HDAC4) expression. Furthermore, rescue experiments revealed that PTPRG-AS1 knockdown-mediated effects on EOC cells were, in part, counteracted by the inhibition of miR-545-3p or restoration of HDAC4.Conclusions: PTPRG-AS1 functioned as an oncogenic lncRNA that aggravated the malignancy of EOC through the miR-545-3p/HDAC4 ceRNA network. Thus, targeting the PTPRG-AS1/miR-545-3p/HDAC4 pathway may be a novel strategy for EOC anticancer therapy.


2018 ◽  
Author(s):  
Marwa Asem ◽  
Allison Young ◽  
Carlysa Oyama ◽  
Rebecca Burkhalter ◽  
Steven Buechler ◽  
...  

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