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Non-thermal plasma induces mitochondria-mediated apoptotic signaling pathway via ROS generation in HeLa cells.
- Source :
-
Archives of biochemistry and biophysics [Arch Biochem Biophys] 2017 Nov 01; Vol. 633, pp. 68-77. Date of Electronic Publication: 2017 Sep 09. - Publication Year :
- 2017
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Abstract
- Non-thermal plasma (NTP) has been proposed as a novel therapeutic method for anticancer treatment. Although increasing evidence suggests that NTP selectively induces apoptosis in some types of tumor cells, the molecular mechanisms underlying this phenomenon remain unclear. In this study, we further investigated possible molecular mechanisms for NTP-induced apoptosis of HeLa cells. The results showed that NTP exposure significantly inhibited the growth and viability of HeLa cells. Morphological observation and flow cytometry analysis demonstrated that NTP exposure induced HeLa cell apoptosis. NTP exposure also activated caspase-9 and caspase-3, which subsequently cleaved poly (ADP- ribose) polymerase. Furthermore, NTP exposure suppressed Bcl-2 expression, enhanced Bax expression and translocation to mitochondria, activated mitochondria-mediated apoptotic pathway, followed by the release of cytochrome c. Further studies showed that NTP treatment led to ROS generation, whereas blockade of ROS generation by N-acetyl-l-cysteine (NAC, ROS scavengers) significantly prevented NTP-induced mitochondrial alteration and subsequent apoptosis of HeLa cells via suppressing Bax translocation, cytochrome c and caspase-3 activation. Taken together, our results indicated that NTP exposure induced mitochondria-mediated intrinsic apoptosis of HeLa cells was activated by ROS generation. These findings provide insights to the therapeutic potential and clinical research of NTP as a novel tool in cervical cancer treatment.<br /> (Copyright © 2017. Published by Elsevier Inc.)
- Subjects :
- Acetylcysteine pharmacology
Apoptosis genetics
Caspase 3 genetics
Caspase 3 metabolism
Caspase 9 genetics
Caspase 9 metabolism
Cell Proliferation drug effects
Cytochromes c metabolism
HeLa Cells
Humans
Mitochondria metabolism
Mitochondria pathology
Plasma Gases antagonists & inhibitors
Poly(ADP-ribose) Polymerases genetics
Poly(ADP-ribose) Polymerases metabolism
Protein Transport drug effects
Proto-Oncogene Proteins c-bcl-2 antagonists & inhibitors
Proto-Oncogene Proteins c-bcl-2 genetics
Proto-Oncogene Proteins c-bcl-2 metabolism
Reactive Oxygen Species metabolism
Signal Transduction
bcl-2-Associated X Protein agonists
bcl-2-Associated X Protein genetics
bcl-2-Associated X Protein metabolism
Antineoplastic Agents pharmacology
Apoptosis drug effects
Gene Expression Regulation, Neoplastic
Mitochondria drug effects
Plasma Gases pharmacology
Reactive Oxygen Species agonists
Subjects
Details
- Language :
- English
- ISSN :
- 1096-0384
- Volume :
- 633
- Database :
- MEDLINE
- Journal :
- Archives of biochemistry and biophysics
- Publication Type :
- Academic Journal
- Accession number :
- 28893509
- Full Text :
- https://doi.org/10.1016/j.abb.2017.09.005