scholarly journals Antizyme inhibitor 1: a potential carcinogenic molecule

2017 ◽  
Vol 108 (2) ◽  
pp. 163-169 ◽  
Author(s):  
Shiqiao Qiu ◽  
Jing Liu ◽  
Feiyue Xing
Amino Acids ◽  
2013 ◽  
Vol 46 (3) ◽  
pp. 575-583 ◽  
Author(s):  
Yasuko Murakami ◽  
Makiko Ohkido ◽  
Hiroko Takizawa ◽  
Noriyuki Murai ◽  
Senya Matsufuji

Author(s):  
Daryl Jin Tai Tay ◽  
Yangyang Song ◽  
Boya Peng ◽  
Tan Boon Toh ◽  
Lissa Hooi ◽  
...  

Tumor Biology ◽  
2017 ◽  
Vol 39 (8) ◽  
pp. 101042831770000 ◽  
Author(s):  
Xueda Hu ◽  
Jingyi Chen ◽  
Xiaoshun Shi ◽  
Fenglan Feng ◽  
King Wai Lau ◽  
...  

RNA editing is a widespread post-transcriptional mechanism that confers specific and reproducible nucleotide changes in selected RNA transcripts and plays a critical role in many human cancers. However, little is known about how RNA editing operates in non-small-cell lung cancers. Here, we measured the sequence and expression level of genes of antizyme inhibitor 1 and adenosine deaminase acting on RNA family in 30 non-small-cell lung cancer patient samples and 13 cell lines and revealed RNA editing S367G in antizyme inhibitor 1 is a high-frequent molecular events. We determined overexpression of antizyme inhibitor 1 with RNA editing, implying the oncogenic function of this alteration. We also detected the association of adenosine deaminase acting on RNA overexpression with RNA editing occurred in antizyme inhibitor 1. Furthermore, the RNA editing could cause a cytoplasmic-to-nuclear translocation of antizyme inhibitor 1 protein and conferred the malignant phenotype of non-small-cell lung cancer cells. The in vivo experiment confirmed that this RNA editing confers higher capacity of tumor migration as well. In conclusion, antizyme inhibitor 1 RNA editing and its involvement in tumorigenesis of non-small-cell lung cancer pave a new way for potential clinical management of non-small-cell lung cancer.


Author(s):  
Cheng‑Hsu Chen ◽  
Yeh‑Han Wang ◽  
Shang‑Feng Tsai ◽  
Tung‑Min Yu ◽  
Shih‑Yin Chen ◽  
...  

1982 ◽  
Vol 204 (3) ◽  
pp. 647-652 ◽  
Author(s):  
K Fujita ◽  
Y Murakami ◽  
S Hayashi

A macromolecular factor that inhibits the activity of the antizyme to ornithine decarboxylase (ODC) was found in rat liver extracts. The factor, ‘antizyme inhibitor’, was heat-labile, non diffusable and of similar molecular size to ODC. The antizyme inhibitor re-activated ODC that had been inactivated by antizyme, apparently by replacing ODC in a complex with antizyme. Therefore the antizyme inhibitor can be used to assay the amount of inactive ODC-antizyme complex formed in vitro. When assayed by this method, the complex was shown to be eluted before ODC from a Sephadex G-100 column. Significant increase in ODC activity was observed when the antizyme inhibitor was added to crude liver extracts from rats that had been injected with 1,3-diaminopropane to cause decay of ODC activity, suggesting the presence of inactive ODC-antizyme complex in the extracts.


PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e69188 ◽  
Author(s):  
Carlos López-Garcia ◽  
Bruno Ramos-Molina ◽  
Ana Lambertos ◽  
Andrés J. López-Contreras ◽  
Asunción Cremades ◽  
...  

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