Abstract

Human colorectal cancer cell lines (HT29 and HCT116) were exposed to dielectric barrier discharge (DBD) plasma at atmospheric pressure to investigate the anticancer capacity of the plasma. The dose- and time-dependent effects of DBDP on cell viability, regulation of transcription factor Sp1, cell-cycle analysis, and colony formation were investigated by means of MTS assay, DAPI staining, propidium iodide staining, annexin V–FITC staining, Western blot analysis, RT-PCR analysis, fluorescence microscopy, and anchorage-independent cell transformation assay. By increasing the duration of plasma dose times, significant reductions in the levels of both Sp1 protein and Sp1 mRNA were observed in both cell lines. Also, expression of negative regulators related to the cell cycle (such as p53, p21, and p27) was increased and of the positive regulator cyclin D1 was decreased, indicating that the plasma treatment led to apoptosis and cell-cycle arrest. In addition, the sizes and quantities of colony formation were significantly suppressed even though two cancer promoters, such as TPA and epidermal growth factor, accompanied the plasma treatment. Thus, plasma treatment inhibited cell viability and colony formation by suppressing Sp1, which induced apoptosis and cell-cycle arrest in these two human colorectal cancer cell lines.

Highlights

  • Particles and ultraviolet (UV) radiation are generated in Cold atmospheric-pressure plasmas (CAPs) and can affect living cells

  • We investigated the effect of Petri dish sized DBD (PDBD) on transcription factor Sp1 in the human Colorectal cancer (CRC) cell lines HT29 and HCT116 to evaluate the anticancer capacity of such treatment depending on dose times

  • We assessed the electrical characteristics of PDBD to determine the optimal conditions for treating CRC cells, as well as the rotational temperature, considering that the gas temperature at atmospheric pressure can be measured by means of OH molecular emission spectra analysis

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Summary

Introduction

Particles (e.g., electrons and ions) and ultraviolet (UV) radiation are generated in CAPs and can affect living cells. Atorvastatin, γ-tocotrienol, and celecoxib are reported to have a synergistic effect on human CRC cells in which they inhibit cancer cell growth by inducing G0/G1-phase cell-cycle arrest and apoptosis[34]. Transcription factor Sp1 playing an important role as basal transcription factor is a protein involved in cell-cycle progression and apoptotic cell death[14,15] These studies suggest that plasma, being rich in ROS, may represent an important gateway to treating cancer. We investigated the effect of PDBD on transcription factor Sp1 in the human CRC cell lines HT29 and HCT116 to evaluate the anticancer capacity of such treatment depending on dose times. The antitumor effect of PDBD was supported by the changes in colony size when two tumor promoters, tetradecanoyl phorbol acetate (TPA) and epidermal growth factor (EGF), were injected into the CRC cells

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