scholarly journals Potential biological process of X‑linked inhibitor of apoptosis protein in renal cell carcinoma based upon differential protein expression analysis

2017 ◽  
Author(s):  
Chao Chen ◽  
Si Cong Zhao ◽  
Wen Zheng Yang ◽  
Zong Ping Chen ◽  
Yong Yan
Keyword(s):  
Renal Cell Carcinoma ◽  
Protein Expression ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Biological Process ◽  
Inhibitor Of Apoptosis ◽  
Differential Protein Expression ◽  
Inhibitor Of Apoptosis Protein ◽  
Differential Protein ◽  
Apoptosis Protein

scholarly journals Expression of inhibitor of apoptosis protein Livin in renal cell carcinoma and non-tumorous adult kidney

2007 ◽  
Vol 97 (9) ◽  
pp. 1271-1276 ◽  
Author(s):  
N Wagener ◽  
I Crnković-Mertens ◽  
C Vetter ◽  
S Macher-Göppinger ◽  
J Bedke ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Inhibitor Of Apoptosis ◽  
Inhibitor Of Apoptosis Protein ◽  
Adult Kidney ◽  
Apoptosis Protein

775 Analysis of differential protein expression between clear cell and chromophobe renal cell carcinoma: Specific biomarkers identification

2015 ◽  
Vol 14 (2) ◽  
pp. e775-e775b
Author(s):  
V. Díez Nicolás ◽  
Cañás I. Ruppen ◽  
V. Gómez Dos Santos ◽  
P. Ximénez-Embún ◽  
Torrecuadrada J. Martínez ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Protein Expression ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Clear Cell ◽  
Chromophobe Renal Cell Carcinoma ◽  
Differential Protein Expression ◽  
Differential Protein

The Inhibitor of apoptosis protein Livin in renal cell carcinoma (RCC)

2008 ◽  
Vol 01 (03) ◽  
Author(s):  
N Wagener ◽  
I Crnkovic-Mertens ◽  
K Hoppe-Seyler ◽  
S Macher-Goeppinger ◽  
A Haferkamp ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Inhibitor Of Apoptosis ◽  
Inhibitor Of Apoptosis Protein ◽  
Apoptosis Protein

scholarly journals Downregulation of lncRNA ZNF582-AS1 due to DNA hypermethylation promotes clear cell renal cell carcinoma growth and metastasis by regulating the N(6)-methyladenosine modification of MT-RNR1

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Wuping Yang ◽  
Kenan Zhang ◽  
Lei Li ◽  
Yawei Xu ◽  
Kaifang Ma ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Renal Cell Carcinoma ◽  
Protein Expression ◽  
Cell Carcinoma ◽  
Clinical Significance ◽  
Renal Cell ◽  
Clear Cell ◽  
Expression Level ◽  
Cell Renal Cell Carcinoma ◽  
Qrt Pcr

Abstract Background Emerging evidence confirms that lncRNAs (long non-coding RNAs) are potential biomarkers that play vital roles in tumors. ZNF582-AS1 is a novel lncRNA that serves as a potential prognostic marker of cancers. However, the specific clinical significance and molecular mechanism of ZNF582-AS1 in ccRCC (clear cell renal cell carcinoma) are unclear. Methods Expression level and clinical significance of ZNF582-AS1 were determined by TCGA-KIRC data and qRT-PCR results of 62 ccRCCs. DNA methylation status of ZNF582-AS1 promoter was examined by MSP, MassARRAY methylation and demethylation analysis. Gain-of-function experiments were conducted to investigate the biological roles of ZNF582-AS1 in the phenotype of ccRCC. The subcellular localization of ZNF582-AS1 was detected by RNA FISH. iTRAQ, RNA pull-down and RIP-qRT-PCR were used to identify the downstream targets of ZNF582-AS1. rRNA MeRIP-seq and MeRIP-qRT-PCR were utilized to examine the N(6)-methyladenosine modification status. Western blot and immunohistochemistry assays were used to determine the protein expression level. Results ZNF582-AS1 was downregulated in ccRCC, and decreased ZNF582-AS1 expression was significantly correlated with advanced tumor stage, higher pathological stage, distant metastasis and poor prognosis. Decreased ZNF582-AS1 expression was caused by DNA methylation at the CpG islands within its promoter. ZNF582-AS1 overexpression inhibited cell proliferative, migratory and invasive ability, and increased cell apoptotic rate in vitro and in vivo. Mechanistically, we found that ZNF582-AS1 overexpression suppressed the N(6)-methyladenosine modification of MT-RNR1 by reducing rRNA adenine N(6)-methyltransferase A8K0B9 protein level, resulting in the decrease of MT-RNR1 expression, followed by the inhibition of MT-CO2 protein expression. Furthermore, MT-RNR1 overexpression reversed the decreased MT-CO2 expression and phenotype inhibition of ccRCC induced by increased ZNF582-AS1 expression. Conclusions This study demonstrates for the first time that ZNF582-AS1 functions as a tumor suppressor gene in ccRCC and ZNF582-AS1 may serve as a potential biomarker and therapeutic target of ccRCC.

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