scholarly journals piRNA-31115 Promotes Cell Proliferation and Invasion via PI3K/AKT Pathway in Clear Cell Renal Carcinoma

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Xinghua Du ◽  
Haomin Li ◽  
Xuexia Xie ◽  
Liping Shi ◽  
Fan Wu ◽  
...  

PIWI-interacting RNAs (piRNAs) are small noncoding RNAs that play important roles in germline development and carcinogenesis. In this study, we used the deep sequencing of small RNA Transcriptome to explore the piRNA expression in six clear cell renal carcinoma (ccRCC) tissues and matched adjacent normal tissues and found that six piRNAs were upregulated and sixteen were downregulated in ccRCC tissues. Among them, piRNA-31115 (NCBI accession number: DQ571003) was the most upregulated piRNA in ccRCC tissues compared with matched adjacent normal tissues. Quantitative real-time PCR (qRT-PCR) was used to confirm piR-31115 expression in other ccRCC tissues ( n = 40 ) and ccRCC cell lines. Besides, function analysis demonstrated that silencing of piR-31115 inhibited ccRCC cell proliferation, motility, and invasiveness. Mechanistic investigations showed that piRNA-31115 may activate epithelial-mesenchymal transition (EMT) via the PI3K/AKT signaling pathway. Hence, piR-31115 may represent an oncogene in the development of ccRCC.

Oncotarget ◽  
2014 ◽  
Vol 6 (4) ◽  
pp. 2193-2205 ◽  
Author(s):  
Nathaniel Weygant ◽  
Dongfeng Qu ◽  
Randal May ◽  
Ryan M. Tierney ◽  
William L. Berry ◽  
...  

2021 ◽  
Vol 11 ◽  
Author(s):  
Li-Xin Ren ◽  
Bo-Wen Zeng ◽  
Meng Zhu ◽  
An-Ning Zhao ◽  
Bei Shi ◽  
...  

Zinc-finger protein 304 (ZNF304) plays a critical role in silencing genes through transcription, regulating cell survival, proliferation, apoptosis, and differentiation during development. However, the roles of transcription factor ZNF304 and its clinical significance in clear cell renal carcinoma (ccRCC) remain unclear. In this study, we found that the expression of ZNF304 was downregulated in ccRCC tissues. Lower levels of ZNF304 were correlated with poor survival. Downregulation of ZNF304 promoted ccRCC cell growth in vitro, whereas overexpression of ZNF304 inhibited growth. Our results indicated that miR-183-5p/FOXO4 mediated ZNF304 regulation of cell growth. Interestingly, we revealed that ZNF304 promoted FOXO4 expression in ccRCC cells. Mechanistically, ZNF304 binds to miR-183 promoter and inhibits miR-183-5p transcription. Furthermore, the expression of miR-183-5p wes increased in ccRCC tissues, and the upregulation of miR-183-5p was related to the poor prognosis of ccRCC patients. miR-183-5p upregulation repressed the expression of FOXO4 and promoted ccRCC progression. These results demonstrated that ZNF304/miR-183-5p/FOXO4 axis played essential role in promoting ccRCC progression, which suggests that disruption of this axis may be a potential therapeutic target in ccRCC.


2004 ◽  
Vol 171 (4S) ◽  
pp. 436-436 ◽  
Author(s):  
Hyung L. Kim ◽  
David B. Seligson ◽  
Nicolette Janzen ◽  
Matthew H. Bui ◽  
Robert A. Figlin ◽  
...  

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