scholarly journals Circular RNA Hsa_circRNA_101996 promotes the development of Gastric Cancer via Upregulating Matrix Metalloproteinases-2/Matrix Metalloproteinases-9 through MicroRNA-143/Ten-eleven translocation-2 Pathway

2021 ◽  
Vol 12 (22) ◽  
pp. 6665-6675
Author(s):  
Feng Huang ◽  
Jiajia Jiang ◽  
Yongliang Yao ◽  
Shiyue Hu ◽  
He Wang ◽  
...  

2021 ◽  
Vol 57 (5) ◽  
pp. 607-619
Author(s):  
L. F. Gallyamova ◽  
A. Kh. Nurgalieva ◽  
I. I. Khidiyatov ◽  
T. R. Nasibullin ◽  
F. R. Munasypov ◽  
...  


2021 ◽  
Vol 11 ◽  
Author(s):  
Dejun Yang ◽  
Zunqi Hu ◽  
Yu Zhang ◽  
Xin Zhang ◽  
Jiapeng Xu ◽  
...  

Circular RNA is a kind of RNA with a covalently closed loop, which has a complex ability to modulate genes in the process of tumorigenesis and metastasis. Nevertheless, how circular RNA functions in gastric cancer (GC) remains unclear. The effect of circHIPK3 in vitro was studied here. Quantitative real-time PCR (qRT-PCR) was employed to found that circHIPK3 markedly increased in GC tissues and cell lines. And low expression of circHIPK3 suppressed the GC cells growing and metabolizing. Then the bioinformatics tool predicted the downstream target of circHIPK3, and it was proved by the dual-luciferase report experiment. According to the results of bioinformatics analysis and experimental data, it was clarified that circHIPK3 acted as a sponge of miR-637, releasing its direct target AKT1. The dual-luciferase assay revealed that mir-637 could bind circHIPK3 and AKT1. qRT-PCR data indicated that overexpression circHIPK3 led to the low level of miR-637 and overexpressed miR-637 would reduce AKT1 level. Finally, we demonstrated that the low expression of miR-637 or overexpression of AKT1 could attenuate the anti-proliferative effects of si-circHIPK3. These results suggest that the circHIPK3/miR-637/AKT1 regulatory pathway may be associated with the oncogene and growth of gastric cancer. In short, a new circular RNA circHIPK3 and its function are identified, and the regulatory pathway of circHIPK3/miR-637/AKT1 in the tumorigenesis and development of gastric cancer is discovered.



2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Zhen Zhang ◽  
Honglei Wu ◽  
Zhaosheng Chen ◽  
Guangchun Li ◽  
Bin Liu


2016 ◽  
Vol 34 (7) ◽  
pp. 305-312 ◽  
Author(s):  
Marta Łukaszewicz-Zając ◽  
Maciej Szmitkowski ◽  
Ala Litman-Zawadzka ◽  
Barbara Mroczko


2021 ◽  
Vol 26 (1) ◽  
Author(s):  
An Yang ◽  
Xin Liu ◽  
Ping Liu ◽  
Yunzhang Feng ◽  
Hongbo Liu ◽  
...  

Abstract Background Long noncoding RNA (lncRNA), urothelial carcinoma-associated 1 (UCA1) is aberrantly expressed in multiple cancers and has been verified as an oncogene. However, the underlying mechanism of UCA1 in the development of gastric cancer is not fully understood. In the present study, we aimed to identify how UCA1 promotes gastric cancer development. Methods The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) data were used to analyze UCA1 and myosin VI (MYO6) expression in gastric cancer. Western blot and quantitative real-time PCR (QPCR) were performed to test the expression level of the UCA1/miR-145/MYO6 axis in gastric cancer cell lines and tissues. The roles of the UCA1/miR-145/MYO6 axis in gastric cancer in vitro and in vivo were investigated by CCK-8 assay, flow cytometry, siRNAs, immunohistochemistry, and a mouse xenograft model. The targeted relationship among UCA1, miR-145, and MYO6 was predicted using LncBase Predicted v.2 and TargetScan online software, and then verified by luciferase activity assay and RNA immunoprecipitation. Results UCA1 expression was higher but miR-145 expression was lower in gastric cancer cell lines or tissues, compared to the adjacent normal cell line or normal tissues. Function analysis verified that UCA1 promoted cell proliferation and inhibited cell apoptosis in the gastric cancer cells in vitro and in vivo. Mechanistically, UCA1 could bind directly to miR-145, and MYO6 was found to be a downstream target gene of miR-145. miR-145 mimics or MYO6 siRNAs could partly reverse the effect of UCA1 on gastric cancer cells. Conclusions UCA1 accelerated cell proliferation and inhibited cell apoptosis through sponging miR-145 to upregulate MYO6 expression in gastric cancer, indicating that the UCA1/miR-145/MYO6 axis may serve as a potential therapeutic target for gastric cancer.





2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Weixin Bian ◽  
Zhiqiang Liu ◽  
Yanjie Chu ◽  
Xiaofang Xing




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