scholarly journals Overexpression of RKIP Inhibits Cell Invasion in Glioma Cell Lines through Upregulation of miR-98

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Zigui Chen ◽  
Quan Cheng ◽  
Zhiming Ma ◽  
Haipeng Xi ◽  
Renjun Peng ◽  
...  

Raf-1 kinase inhibitor protein (RKIP) is a tumor and metastasis suppressor in cancer cells. MicroRNAs (miRNAs) have been suggested to play a vital role in tumor initiation and progression by negatively regulating oncogenes and tumor suppressors. Quite recently, studies have identified some miRNAs operating to promote or suppress tumor invasion or metastasis via regulating metastasis-related genes, providing potential therapeutic targets on antimetastasis strategy. In this study, we found that the expression of RKIP and miR-98 in glioma tissues were significantly lower than that in normal brain tissues. Overexpression of RKIP upregulated miR-98 expression and inhibited glioma cell invasion and miR-98 target gene HMGA2 but had no effect in glioma cell proliferation. Moreover, forced expression of miR-98 accelerated the inhibition of glioma cell invasion and the expression of HMGA2 also had no effect in glioma cell proliferation. Our findings newly described RKIP/miR-98 to HMGA2 link and provided a potential mechanism for glioma cell invasion. RKIP and miR-98 may illustrate the potential therapeutic utility of signaling pathway signatures.

2015 ◽  
Vol 71 ◽  
pp. 7-14 ◽  
Author(s):  
Jihong Zhang ◽  
Xuhai Gong ◽  
Kaiyu Tian ◽  
Dongkai Chen ◽  
Jiahang Sun ◽  
...  

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e77299 ◽  
Author(s):  
Mohammad A. Y. Alqudah ◽  
Supreet Agarwal ◽  
Maha S. Al-Keilani ◽  
Zita A. Sibenaller ◽  
Timothy C. Ryken ◽  
...  

2005 ◽  
Vol 74 (3) ◽  
pp. 233-239 ◽  
Author(s):  
Tsuyoshi Suzuki ◽  
Shuichi Izumoto ◽  
Kouichi Wada ◽  
Yasunori Fujimoto ◽  
Motohiko Maruno ◽  
...  

2018 ◽  
Vol 46 (3) ◽  
pp. 1055-1064 ◽  
Author(s):  
Xin Chen ◽  
Deheng Li ◽  
Yang Gao ◽  
Wei Tang ◽  
Lao IW ◽  
...  

Background/Aims: Long noncoding RNAs (lncRNAs) are a novel class of protein-noncoding transcripts that are aberrantly expressed in multiple diseases including cancers. LINC00152 has been identified as an oncogene involved in many kinds of cancer; however, its expression pattern and function in human glioma remain unclear. Methods: Quantitative real-time polymerase chain reaction was carried out to measure LINC00152 expression in human glioma cell lines and tissues. CCK-8 and EdU assays were performed to assess cell proliferation, and scratch assays and Transwell assays were used to assess cell migration and invasion, respectively. Luciferase reporter assays were carried out to determine the interaction between miR-16 and LINC00152. In vivo experiments were conducted to assess tumor formation. Results: LINC00152 was found to be significantly upregulated in human glioma cell lines and clinical samples. Knockdown of LINC00152 suppressed glioma cell proliferation, migration, and invasion in vitro. In vivo assays in nude mice confirmed that LINC00152 knockdown inhibits tumor growth. Furthermore, mechanistic investigation showed that LINC00152 binds to miR-16 in a sequence-specific manner and suppresses its expression. miR-16 inhibition strongly attenuated LINC00152 knockdown–mediated suppressive effects on proliferation, migration, and invasion. Moreover, LINC00152 induced BMI1 expression by sponging miR-16; this effect further promoted glioma cell proliferation and invasion. Conclusion: We regard LINC00152 as an oncogenic lncRNA promoting glioma cell proliferation and invasion and as a potential target for human glioma treatment.


Neuroreport ◽  
2020 ◽  
Vol 32 (1) ◽  
pp. 52-60
Author(s):  
Jian Wen ◽  
Xin Li ◽  
Yan Ding ◽  
Shaohua Zheng ◽  
Ying Xiao

Sign in / Sign up

Export Citation Format

Share Document