Abstract
<p class="Abstract">The objective of this study was to evaluate the role of poly (ADP-ribose) polymerase-1 (PARP-1) and NF-kappaB as potential risk factor in the development of non-small cell lung cancer in Chinese individuals (n=110) of either gender aged &lt;65 years. Healthy Chinese individuals (n=110) were included as control. Polymerase chain reaction was used to determine the role of PART-1 and NF-kappaB using plasma sample. The individuals with the GA genotype and carrier of G allele were at high-risk of non-small cell lung cancer. There was involvement of dL/is of the NF-kappaB in non-small cell lung cancer. Our study result suggests that the PARP-1 and NF-kappaB play an important role in development of non-small cell lung cancer in China.</p>
Highlights
Lung cancer is one of the important causes of mortality worldwide (Park et al, 2015; Masuda et al, 2015)
(ADP-ribose) polymerase-1 (PARP-1) is known as adenosine diphosphate-ribosyltransferases catalyses the process of PARylation by attaching the polymers of ADP-ribose on target protein motif via ester linkage and trigger the array of vital cellular functions viz. chromatin structure, DNA repair, transcriptional regulation, apoptosis, necrosis, cell separation and differentiation
17 members of Poly (ADP-ribose) polymerase-1 (PARP-1) are expressed, of which NAD+ ADP-ribosyltransferase is associated with the nucleus and regulates at least 85% of the cellular NAD+ ADP-ribosyltransferase activities (Hur et al, 2006; Smulson et al, 2000; Corcoran et al, 2016; Hassa et al, 2008; Phulwani et al, 2008)
Summary
Lung cancer is one of the important causes of mortality worldwide (Park et al, 2015; Masuda et al, 2015). Most patients with non-small cell lung cancer are diagnosed at the advanced stages (stages IIIb and IV), with only 16-30% diagnosed in the early stages of the disease (Park et al, 2015; Masuda et al, 2015; Polanski et al, 2016). Patients diagnosed with advanced non-small cell lung cancer generally have a poor prognosis, with a median survival of 8-10 months and 2 and 5-year survival rates of approximately 20% and 15%, respectively (Park et al, 2015; Masuda et al, 2015; Polanski et al, 2016; Ali et al, 2013). Throughout the cellular and/or genotoxic stress, prolong activation of
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