Abstract

<p>The present study evaluated the anti-proliferative and apoptotic effect of quinine on oral cancer cells Hep-2 and KB. Cell inhibition, apoptosis and anti-inflammatory effects were explored by nuclear DNA cleavage, condensation, change in membrane potential of mitochondria. Meanwhile, inflammatory and apoptosis-related mRNA and proteins expressions such as iNOS COX-2, IL-6, Bcl-2, mutant p53, Bax, caspase-3 and NF-κB were determined by RT-PCR and Western blotting assays. Results showed that, quinine treatment significantly inhibited the cell viability and colony formation, inhibited cell proliferation lead to increased generation of reactive oxygen species induction of MMP depolarization, morphological changes and DNA damage in dose- and time-dependent manner. Moreover, quinine significantly decreased the iNOS, COX-2, IL-6, Bcl-2 and mutant p53 simultaneously up-regulated Bax, caspase-3 expressions through the inhibition of NF-κB suggest that quinine may serve as a potential candidate in the prevention of cell proliferation and enhances apoptosis via inhibiting up-stream signalling.</p><p><strong>Video Clip</strong></p><p><a href="https://youtube.com/v/83HX2fFTXkg">Programmed cell death assay by dual staining:</a> 17 min 25 sec</p><p> </p>

Highlights

  • Oral cancer is the 6th most common cancer worldwide, reprising 48% of head and neck cancers (O'Callaghan et al, 2015)

  • The generation of Reactive oxygen species (ROS) in Hep-2 and KB was studied in control as well as in treatment with quinine (Figure 1)

  • Changes of mitochondrial membrane potential in Hep-2 and KB cells were observed when treated with quinine (Figures 2)

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Summary

Introduction

Oral cancer is the 6th most common cancer worldwide, reprising 48% of head and neck cancers (O'Callaghan et al, 2015). Apart from inflammation p53, Bcl-2, Bax and caspase-3 are major mediators for proand anti-apoptotic mechanism that is essential for treatment with anti-cancer chemotherapies through apoptosis (Li et al, 2015; Bi et al, 2015). Each of these pro-inflammatory and anti-apoptotic genes were activated response of several transcription factors. Nuclear factor kappa B gain attention in the treatment of several inflammatory diseases (Kim et al, 2013; Shou et al, 2002)

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