scholarly journals Long Noncoding RNA CRNDE Promotes Proliferation of Gastric Cancer Cells by Targeting miR-145

2017 ◽  
Vol 42 (1) ◽  
pp. 13-21 ◽  
Author(s):  
Cheng En Hu ◽  
Pei Zhun Du ◽  
Hui Dong Zhang ◽  
Guang Jian Huang

Background/Aims: The colorectal neoplasia differentially expressed (CRNDE) gene is a long noncoding RNA (lncRNAs) that is upregulated in colorectal cancer and glioma. Here, we investigated the regulatory function of CRNDE in gastric cancer (GC). Methods: CRNDE and miR-145 expression were assayed by qRT-PCR, and E2F3 protein expression was measured by western blotting. A luciferase reporter assay was used to detect the direct regulation of miR-145 by CRNDE. Cell viability and colony formation of human GC cells were detected using MTT and colony formation assay, respectively. Results: CRNDE was highly expressed in GC cell lines and tissues; overexpression of CRNDE increased GC cell viability and promoted colony formation. Knockdown of CRNDE did not result in loss of expression-related effects on cell proliferation and colony formation. Further investigation revealed that the miR-145 target gene E2F3 was strongly expressed following CRNDE competitive molecular sponging of miR-145. Conclusion: CRNDE acted as a growth-promoting lncRNA in GC and maybe a potential target of GC treatment.

Oncotarget ◽  
2016 ◽  
Vol 8 (24) ◽  
pp. 38227-38238 ◽  
Author(s):  
Fengqi Nie ◽  
Xiang Yu ◽  
Mingde Huang ◽  
Yunfei Wang ◽  
Min Xie ◽  
...  

2020 ◽  
Vol 19 (9) ◽  
pp. 1821-1826
Author(s):  
Xiaosheng Jin ◽  
Peipei Cai ◽  
Zhengchao Shi ◽  
Fangpeng Ye ◽  
Tingting Ji ◽  
...  

Purpose: Gastric cancer (GC) is one of the most frequent tumors with high mortality rate, worldwide. A proper understanding of the mechanism  underlying its progression is required for its diagnosis and development of novel treatment option. MicroRNAs are associated with the development and advancement of different types of cancer, including GC. The current research was aimed at investigating the molecular and biological function of miR-148a-3p in GC development.Methods: A human normal gastric epithelial cell line, GES-1 (control) as well as four GC cell lines (NUGC-4, SNU-520, STKM-2 and MKN-74) were employed for the study. MiR-148a-3p and ATP6AP2 expression levels in GC cell lines were examined by RT-qPCR technique. Transfection procedure was used to upregulate miR-148a-3p expression in the MKN-45 cell line. MTT assay was utilized to evaluate cell viability in GC cell lines. The molecular interaction between miR-148a-3p and ATP6AP2 was predicted using bioinformatics system and the prediction was then validated by luciferase reporter assay.Results: Expression levels of miR-148-3p was low, whilst that of ATP6AP2 was high in GC cell lines. MiR-148a-3p overexpression resulted in the reduction of cell viability in GC cell lines. More so, it was confirmed that miR-148-3p, as a post-transcriptional regulator inhibited ATP6AP2 expression by having a negative association with it in GC cells. More so, ATP6AP2 was found to be a direct target of miR-148a-3p.Conclusion: Our results revealed that miR-148a-3p plays a crucial function in GC development through targeting ATP6AP2. This finding could be explored in the discovery of new therapeutic approaches for GC treatment. Keywords: ATP6AP2, Cell viability, Gastric cancer, miR-148a-3p, Progression


PLoS ONE ◽  
2017 ◽  
Vol 12 (8) ◽  
pp. e0182433 ◽  
Author(s):  
Jun Cai ◽  
Dong Wang ◽  
Zhi-Gang Bai ◽  
Jie Yin ◽  
Jun Zhang ◽  
...  

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Ying Jiang ◽  
Shan Jin ◽  
Shisheng Tan ◽  
Yingbo Xue ◽  
Xue Cao

Abstract Background Long noncoding RNA nuclear-enriched abundant transcript 1 (NEAT1) exhibits an oncogenic role in multiple cancers, including gastric cancer (GC). But, the functions of NEAT1 in modulating radio-sensitivity of GC and its potential molecular mechanisms have not been totally elucidated. Methods qRT-PCR was performed to detect the expressions of NEAT1 and microRNA-27b-3p (miR-27b-3p). Kaplan–Meier survival curves for NEAT1 expression in GC created using KM Plotter. Colony formation assay was used to determine the survival fraction. Cell apoptosis was evaluated by flow cytometry. Luciferase reporter assay was used to verify the relationship between miR-27b-3p and NEAT1. Results NEAT1 was highly expressed while miR-27b-3p was downregulated in GC tissues and cells. NEAT1 was negatively correlated with that of miR-27b-3p and associated with poor overall survival. Moreover, NEAT1 and miR-27b-3p varied inversely after radiation in GC tissues and cells. Loss of NEAT1 or upregulation of miR-27b-3p increased the effect of radiation on cell survival fraction inhibition and apoptosis promotion. In addition, NEAT1 negatively regulated the expression of miR-27b-3p in GC cells. Interestingly, the depletion of miR-27b-3p dramatically attenuated the NEAT1 knockdown-mediated function in AGS and MKN-45 cells treated with radiation in vitro. Similarly, downregulation of NEAT1 enhanced the radiation-mediated inhibition of tumor growth, which was mitigated by decrease of miR-27b-3p. Conclusion NEAT1 depletion enhanced radio-sensitivity of GC by negatively regulating miR-27b-3p in vitro and in vivo.


Gene ◽  
2019 ◽  
Vol 687 ◽  
pp. 116-124 ◽  
Author(s):  
Zhigang Miao ◽  
Xiaozhong Guo ◽  
Liang Tian

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