scholarly journals ALDH2 Repression Promotes Lung Tumor Progression via Accumulated Acetaldehyde and DNA Damage

Neoplasia ◽  
2019 ◽  
Vol 21 (6) ◽  
pp. 602-614 ◽  
Author(s):  
Kaimi Li ◽  
Wenzheng Guo ◽  
Zhanming Li ◽  
Yang Wang ◽  
Beibei Sun ◽  
...  
2007 ◽  
Vol 28 (10) ◽  
pp. 2082-2088 ◽  
Author(s):  
P. G. Nuciforo ◽  
C. Luise ◽  
M. Capra ◽  
G. Pelosi ◽  
F. d'Adda di Fagagna

Author(s):  
Giorgia Foggetti ◽  
Chuan Li ◽  
Hongchen Cai ◽  
Dmitri A. Petrov ◽  
Monte M. Winslow ◽  
...  

Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3333
Author(s):  
Jun Tang ◽  
Víctor Curull ◽  
Xuejie Wang ◽  
Coral Ampurdanés ◽  
Xavier Duran ◽  
...  

(1) Background: Lung cancer (LC) is a major leading cause of death worldwide. Poly (ADP-ribose) polymerase (PARP)-1 and PARP-2 are key players in cancer. We aimed to assess PARP-1 and PARP-2 expression and activity and DNA damage in tumors and non-tumor lungs from patients with/without chronic obstructive pulmonary disease (COPD). (2) Methods: Lung tumor and non-tumor specimens were obtained through video-assisted thoracoscopic surgery (VATS) in LC patients with/without underlying COPD (two groups of patients, n = 15/group). PARP-1 and PARP-2 expression (ELISA), PARP activity (PARP colorimetric assay kit) and DNA damage (immunohistochemistry) levels were identified in all samples. (3) Results: Both PARP-1 and PARP-2 expression levels were significantly lower in lung tumors (irrespective of COPD)compared to non-tumor specimens, while DNA damage and PARP activity levels significantly increased in lung tumors compared to non-tumor specimens only in LC-COPD patients. PARP-2 expression was positively correlated with smoking burden in LC-COPD patients. (4) Conclusions: In lung tumors of COPD patients, an overactivation of PARP enzyme was observed. A decline in PARP-1 and PARP-2 protein expression was seen in lung tumors irrespective of COPD. Other phenotypic features (airway obstruction) beyond cancer may account for the increase in PARP activity seen in the tumors of patients with underlying COPD.


Tumor Biology ◽  
2016 ◽  
Vol 37 (11) ◽  
pp. 15347-15347
Author(s):  
Cheng Ai ◽  
Rujian Jiang ◽  
Li Fu ◽  
Youdong Chen
Keyword(s):  

2020 ◽  
Vol 22 (9) ◽  
pp. 1472-1480
Author(s):  
S. Kashyap ◽  
J. Jha ◽  
M. K. Singh ◽  
L. Singh ◽  
S. Sen ◽  
...  

2013 ◽  
Vol 288 (29) ◽  
pp. 20908-20917 ◽  
Author(s):  
Tanjing Song ◽  
Leixiang Yang ◽  
Neha Kabra ◽  
Lihong Chen ◽  
John Koomen ◽  
...  

The chromosomal region encoding the nuclear NAD+ synthesis enzyme nicotinamide mononucleotide adenylyltransferase (NMNAT1) is frequently deleted in human cancer. We describe evidence that NMNAT1 interacts with the nucleolar repressor protein nucleomethylin and is involved in regulating rRNA transcription. NMNAT1 binds to nucleomethylin and is recruited into a ternary complex containing the NAD+-dependent deacetylase SirT1. NMNAT1 expression stimulates the deacetylase function of SirT1. Knockdown of NMNAT1 enhances rRNA transcription and promotes cell death after nutrient deprivation. Furthermore, NMNAT1 expression is induced by DNA damage and plays a role in preventing cell death after damage. Heterozygous deletion of NMNAT1 in lung tumor cell lines correlates with low expression level and increased sensitivity to DNA damage. These results suggest that NMNAT1 deletion in tumors may contribute to transformation by increasing rRNA synthesis, but may also increase sensitivity to nutrient stress and DNA damage.


2011 ◽  
Vol 108 (44) ◽  
pp. 18061-18066 ◽  
Author(s):  
Q. Gao ◽  
E. J. Steine ◽  
M. I. Barrasa ◽  
D. Hockemeyer ◽  
M. Pawlak ◽  
...  

2014 ◽  
Vol 33 (13) ◽  
pp. 1502-1502 ◽  
Author(s):  
Allison N Lau ◽  
Stephen J Curtis ◽  
Christine M Fillmore ◽  
Samuel P Rowbotham ◽  
Morvarid Mohseni ◽  
...  
Keyword(s):  

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