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 <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)

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Summary

Introduction

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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