Effects of Long Non-Coding RNA RP11-468E2.5 on Cell Proliferation and Apoptosis in Colorectal Cancer Cells by Targeting STAT5 and STAT6 via the JAK/STAT Signaling Pathway

Author(s):  
Yin-Ling Mao ◽  
Xu-Hai Zhao ◽  
Jun-Feng Wang ◽  
Hui-Jun Zheng ◽  
Qing-Shan You ◽  
...  
2017 ◽  
Vol 41 (6) ◽  
pp. 2489-2502 ◽  
Author(s):  
Bo Yu ◽  
Xuan Ye ◽  
Qiong Du ◽  
Bin Zhu ◽  
Qing Zhai

Background/Aims: The long non-coding RNA colorectal neoplasia differentially expressed (CRNDE) contributes to the proliferation and migration of tumors. However, its molecular mechanism underlying gastric cancer remains unknown. In the present study, we investigated whether CRNDE was involved in the development of colorectal cancer via the binding of microRNA (miR)-217 with transcription factor 7-like 2 (TCF7L2) to enhance the Wnt signaling pathway. Methods: Quantitative polymerase chain reaction was used to detect CRNDE, miR-217 and TCF7L2 in colorectal cancer tissues and cells. The CCK-8 assay, wound healing assay, and Transwell assay were used to detect cell proliferation, migration and invasion, respectively. Western blotting and luciferase activity assays were used to identify CRNDE and TCF7L2 as one of the direct targets of miR-217. The activity of the Wnt/β-catenin signaling pathway was analyzed by the TOPflash assay, and the subcellular localization of β-catenin and TCF7L2 was analyzed by western blotting and confocal microscopy. Results: In this study, we found that high expression of CRNDE is negatively correlated with low expression of miR-217 in colorectal cancer tissue and colorectal cancer cells. The dual luciferase reporter analysis showed that miR-217 is bound to CRNDE and TCF7L2 and negatively regulate their expression. CRNDE down-regulation inhibited the cell proliferation, migration and invasion in vitro and in vivo and the inhibitions were both completely blocked after miR-217 inhibition or TCF7L2 overexpression. Finally, TOPflash analysis showed that the activity of Wnt/β-catenin signaling is inhibited by CRNDE down-regulation and rescued by TCF7L2 over-expression. Consistently immunostaining and western blotting analysis showed that the expression of b-catenin and TCF7L2 in the nucleus was significantly decreased by CRNDE down-regulation and was rescued by TCF7L2 over-expression. Conclusions: The present study suggest that CRNDE involves in the cell proliferation, migration and invasion of colorectal cancer cells via increasing the expression of TCF7L2 and activity of Wnt/β-catenin signaling through binding miR-217 competitively.


Life Sciences ◽  
2017 ◽  
Vol 188 ◽  
pp. 37-44 ◽  
Author(s):  
Lei Qiao ◽  
Xiangyu Liu ◽  
Yichao Tang ◽  
Zheng Zhao ◽  
Jilong Zhang ◽  
...  

2019 ◽  
Vol 215 (11) ◽  
pp. 152622 ◽  
Author(s):  
Zhengchun Kang ◽  
E Jifu ◽  
Kai Guo ◽  
Xiuzhu Ma ◽  
Yingyi Zhang ◽  
...  

2020 ◽  
Vol 10 (3) ◽  
pp. 365-370
Author(s):  
Qiupeng Du ◽  
Na Du ◽  
Chenchen Zhu ◽  
Qingqing Shang ◽  
Haiyan Mao ◽  
...  

Objective: To assess whether miR-203 regulates DJ-1 expression, affects colorectal cancer cells through PTEN-PI3K/AKT signaling. Methods: Colorectal cancer (CRC) tissues and adjacent tissues were collected followed by analysis of the level of miR-203, DJ-1 and PTEN. miR-203 and DJ-1 level was measured in HCT116, SW480 and normal colorectal cell NCM460. miR-203 mimic or miR-NC was transfected into HCT116 or SW480 cells followed by measuring the level of miR-203, DJ-1, PTEN, p-AKT as well as cell apoptosis and proliferation. Results: Compared with tumor adjacent tissues, tumor tissues showed significantly lower level of miR-203 and PTEN, and higher level of DJ-1. There is a targeted relationship between miR-203 and DJ-1. Compared with NCM460 cell, HCT116 and SW480 cells displayed significantly lower miR-203 level and higher DJ-1 expression. miR-203 mimic significantly reduced DJ-1 and p-AKT level, increased PTEN expression, cell apoptosis and inhibited cell proliferation. Conclusion: Lower miR-203 and higher DJ-1 level is found in CRC patients. Upregulation of miR-203 inhibits DJ-1 expression, increases PTEN expression, impairs PI3K/AKT signaling, inhibits CRC cell proliferation and promotes apoptosis.


Sign in / Sign up

Export Citation Format

Share Document