scholarly journals SP1-induced upregulation of the long noncoding RNA TINCR regulates cell proliferation and apoptosis by affecting KLF2 mRNA stability in gastric cancer

Oncogene ◽  
2015 ◽  
Vol 34 (45) ◽  
pp. 5648-5661 ◽  
Author(s):  
T-p Xu ◽  
X-x Liu ◽  
R Xia ◽  
L Yin ◽  
R Kong ◽  
...  
2017 ◽  
Vol 8 (6) ◽  
pp. e2839-e2839 ◽  
Author(s):  
Zhen-Qiang Wang ◽  
Qiang Cai ◽  
Lei Hu ◽  
Chang-Yu He ◽  
Jian-Fang Li ◽  
...  

Tumor Biology ◽  
2015 ◽  
Vol 37 (6) ◽  
pp. 7693-7701 ◽  
Author(s):  
Feng-qi Nie ◽  
Shijie Ma ◽  
Min Xie ◽  
Yan-wen Liu ◽  
Wei De ◽  
...  

2018 ◽  
Vol 49 (1) ◽  
pp. 322-334 ◽  
Author(s):  
Jiaojiao Hu ◽  
Yingying Qian ◽  
Lipan Peng ◽  
Ling Ma ◽  
Tianzhu Qiu ◽  
...  

Background/Aims: LncRNA EGFR-AS1 is an antisense transcript of EGFR, which plays a key role in gastric cancer progression. This study was aimed to explore the effects of lncRNA EGFR-AS1 on GC and the underling mechanisms. Methods: The silencing of EGFR-AS1 expression was performed by using EGFR-AS1 shRNA lentivirus in MGC803 and SGC-7901 GC cell. The levels of lncRNA EGFR-AS1 and EGFR were detected by qPCR and western blot. Cell proliferation was assessed by CCK-8, EdU, and colony formation assays. The EGFR mRNA stability was explored by using RNA synthesis inhibitor α-amanitin. Results: In our study, EGFR-AS1 significantly up-regulated in GC tissues and correlated with tumor size. And the expression of EGFR-AS1 positively correlated with EGFR in tissues. Moreover, knock-down of EGFR-AS1 inhibited the proliferation of GC cells via suppressing EGFR-dependent PI3K/AKT pathway in vitro and in vivo. Mechanismly, depletion of EGFR-AS1 was found to decrease EGFR expression by reduction of EGFR mRNA stability. Conclusion: Our findings suggested that EGFR-AS1 might have an oncogenic effect on GC and serve as a potential target of GC.


2017 ◽  
Vol 42 (6) ◽  
pp. 2364-2376 ◽  
Author(s):  
Jin Yan ◽  
Yifeng Zhang ◽  
Qiang She ◽  
Xuan Li ◽  
Lei Peng ◽  
...  

Background: Long noncoding RNA (lncRNA) H19 is emerging as a vital regulatory molecule in the progression of different types of cancer and miR-675 is reported to be embedded in H19's first exon. However, their function and specific mechanisms of action have not been fully elucidated. The aim of this study was to identify a novel lncRNA-microRNA-mRNA functional network in gastric cancer. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to assess the relative expression of H19 and miR-675 in normal (GES-1) and gastric cancer cell lines (SGC-7901, SGC-7901/DDP) as well as in tumor tissues. Gain and loss of function approaches were carried out to investigate the potential roles of H19/miR-675 in cell proliferation and apoptosis. Moreover, Fas associated via death domain (FADD) was validated to be the target of miR-675 via luciferase reporter assay. Western blotting was used to evaluate the protein expression of related signaling pathway. Results: In our study H19 and miR-675 were increased in gastric cancer cell lines and tissues. Overexpression of H19 and miR-675 promoted cell proliferation and inhibited cell apoptosis, whereas knockdown of H19 and miR-675 inhibited these effects. By further examining the underlying mechanism, we showed that H19/miR-675 axis inhibited expression of FADD. FADD downregulation subsequently inhibited the caspase cleavage cascades including caspase 8 and caspase 3. Conclusion: Taken together, our results point to a novel regulatory pathway H19/miR-675/ FADD/caspase 8/caspase 3 in gastric cancer which may be potential target for cancer therapy.


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