miR-206 functions as a novel cell cycle regulator and tumor suppressor in clear-cell renal cell carcinoma

2016 ◽  
Vol 374 (1) ◽  
pp. 107-116 ◽  
Author(s):  
Haibing Xiao ◽  
Wei Xiao ◽  
Jing Cao ◽  
Heng Li ◽  
Wei Guan ◽  
...  
2004 ◽  
Vol 200 (4) ◽  
pp. 277
Author(s):  
K. Struckmann ◽  
P. Schraml ◽  
R. Simon ◽  
K. Elmen-Horst ◽  
M. Mirlacher ◽  
...  

2004 ◽  
Vol 64 (5) ◽  
pp. 1632-1638 ◽  
Author(s):  
Kirsten Struckmann ◽  
Peter Schraml ◽  
Ronald Simon ◽  
Katja Elmenhorst ◽  
Martina Mirlacher ◽  
...  

PLoS ONE ◽  
2016 ◽  
Vol 11 (7) ◽  
pp. e0157599 ◽  
Author(s):  
Weihao Chen ◽  
Shaoxi Niu ◽  
Xin Ma ◽  
Peng Zhang ◽  
Yu Gao ◽  
...  

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Zhuo Ye ◽  
Jiachen Duan ◽  
Lihui Wang ◽  
Yanli Ji ◽  
Baoping Qiao

Abstract Background Clear cell renal cell carcinoma (ccRCC) is the most common renal cell carcinoma subtype with a poor prognosis. LncRNA-LET is a long non-coding RNA (lncRNA) that is down-regulated in ccRCC tissues. However, its role in ccRCC development and progress is unclear. Methods LncRNA-LET expression was detected in ccRCC tissues and ccRCC cells using quantitative real-time PCR. The overexpression and knockdown experiments were performed in ccRCC cells and xenograft mouse model to evaluate role of lncRNA-LET. Cell cycle, apoptosis and JC-1 assays were conducted via flow cytometer. The protein levels were measured through western blot analysis and the interaction between lncRNA-LET and miR-373-3p was identified via luciferase reporter assay. Results LncRNA-LET expression was lower in ccRCC tissues than that in the matched adjacent non-tumor tissues (n = 16). In vitro, lncRNA-LET overexpression induced cell cycle arrest, promoted apoptosis and impaired mitochondrial membrane potential, whereas its knockdown exerted opposite effects. Moreover, we noted that lncRNA-LET may act as a target for oncomiR miR-373-3p. In contrast to lncRNA-LET, miR-373-3p expression was higher in ccRCC tissues. The binding between lncRNA-LET and miR-373-3p was validated. Two downstream targets of miR-373-3p, Dickkopf-1 (DKK1) and tissue inhibitor of metalloproteinase-2 (TIMP2), were positively regulated by lncRNA-LET in ccRCC cells. MiR-373-3p mimics reduced lncRNA-LET-induced up-regulation of DKK1 and TIMP2 levels, and attenuated lncRNA-LET-mediated anti-tumor effects in ccRCC cells. In vivo, lncRNA-LET suppressed the growth of ccRCC xenograft tumors. Conclusion These findings indicate that lncRNA-LET plays a tumor suppressive role in ccRCC by regulating miR-373-3p.


Oncotarget ◽  
2015 ◽  
Vol 6 (6) ◽  
pp. 4066-4079 ◽  
Author(s):  
Wei Xiang ◽  
Jun He ◽  
Chao Huang ◽  
Lejun Chen ◽  
Dan Tao ◽  
...  

2018 ◽  
Vol 22 (7) ◽  
pp. 873-877
Author(s):  
E. A. Klimentova ◽  
I. R. Gilyazova ◽  
A. A. Izmailov ◽  
I. M. Sultanov ◽  
M. A. Bermisheva ◽  
...  

Kidney cancer is a heterogeneous group of malignant tumors, the vast majority of which are renal cell carcinomas (RCC) of various morphological types, of which the most common is the clear cell renal cell carcinoma (ccRCC). Particular attention in the carcinogenesis of the ccRCC is given to a number of tumor suppressor genes located on the short arm of the third chromosome. One of these genes, which are inactivated in the case of ccRCC is the PBRM1 gene encoding the PBAF SWI/SNF subunit of the chromatin remodeling complex, BAF180. The PBRM1 gene is located on the short arm of the third chromosome in the 3p21 region near the von Hippel-Lindau gene (VHL), the mutation in which is the main event in the occurrence of ccRCC. The aim of our investigation is identification of changes in the nucleotide sequence of the PBRM1 tumor suppressor gene in patients with ccRCC. 210 pairs of DNA samples isolated from ccRCC tissue were studied. Analysis of changes in the nucleotide sequence of DNA was carried out by HRM analysis and direct sequencing. In the PBRM1 gene, two somatic mutations were found (c.233G>A (p.D45N) in exon 2, c.1675-1676delTC in exon 15) which were not described previously, and one known polymorphic variant rs17264436 (in exon 23). The frequency of detected mutations was 0.95 % of cases. Analysis of the allelic association for the polymorphic locus rs17264436 showed a statistically significant increase in the risk of developing advanced kidney cancer in carriers of allele rs17264436*A, which can be used in the development of prognostic marker panels. Perhaps the low frequency of mutations in the samples we studied is due to the fact that the inactivation of the PBRM1 gene takes place in other ways, and may also be due to the ethno-specificity of the studied group of patients.


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