Cancers, Vol. 12, Pages 3333: Increased PARP Activity and DNA Damage in NSCLC Patients: The Influence of COPD

Alexandros G.Sfakianakis shared this article with you from Inoreader Cancers, Vol. 12, Pages 3333: Increased PARP Activity and DNA Damage in NSCLC Patients: The Influence of COPD Μέσω Cancers Cancers, Vol. 12, Pages 3333: Increased PARP Activity and DNA Damage in NSCLC Patients: The Influence of COPD Cancers doi: 10.3390/cancers12113333 Authors: Jun Tang Víctor Curull Xuejie Wang Coral Ampurdanés Xavier Duran Lara Pijuan Alberto Rodríguez-Fuster Rafael Aguiló José Yélamos Esther Barreiro (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 expressio n 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. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.