Tumor Biol. (2014) 35:5213–5217 DOI 10.1007/s13277-014-1677-7
RESEARCH ARTICLE
Propofol induces endoplasmic reticulum (ER) stress and apoptosis in lung cancer cell H460 Wen-Yao Cui & Yan Liu & Yong-Qiang Zhu & Tao Song & Qiu-Shi Wang
Received: 18 November 2013 / Accepted: 22 January 2014 / Published online: 9 February 2014 # International Society of Oncology and BioMarkers (ISOBM) 2014
Abstract Propofol is one of the most commonly used intravenous anesthetic agents during cancer resection surgery. It can influence proliferation, motility, and invasiveness of cancer cells in vitro and in vivo. However, the role of the propofol in the lung cancer cells remains unclear. In this study, we demonstrated the effects of propofol on the proliferation and the apoptosis of lung cancer cell H460 by using colony formation assay and flow cytometry. Propofol also decreased tumor size and weight in established xenografted tumors. Furthermore, propofol-induced endoplasmic reticulum (ER) stress was determined by Western blot. Keywords Propofol . Lung cancer . Endoplasmic reticulum . Apoptosis . Caspase
influence proliferation, motility, and invasiveness of cancer cells in vitro and in vivo [6, 7]. Therefore, in this study, we investigated the possible antitumor properties of propofol in lung cancer cell H460 and the underlying mechanisms associated with its activity. Induction of the endoplasmic reticulum (ER) stress pathway known as the unfolded protein response (UPR) is activated in a number of disease processes such as obesity, diabetes, atherosclerosis, and cancer [8, 9]. In the present study, we examined the effect of propofol on lung cancer cells both in vivo and in vitro. We demonstrate that propofol induced apoptosis in H460 cells partly through ER stress.
Materials and methods H460 cell culture and drug exposure
Introduction Lung cancer continues to be the most commonly diagnosed cancer as well as the leading cause of cancer death in the world [1]. Surgery remains a primary treatment for lung cancer. However, the influence of the perioperative factors, such as anesthetic(s), on lung cancer cells was not clear [2]. Propofol (2, 6-diisopropylphenol) is one of the most commonly used intravenous anesthetic agents producing smooth induction and rapid recovery from anesthesia [3]. It produces a variety of pharmacodynamic effects, such as hypnosis to general anesthesia, relaxes amnestic and muscles, and downregulates the production of pro-inflammatory cytokines [4, 5]. Previous studies also showed that propofol can W.
RESEARCH ARTICLE
Propofol induces endoplasmic reticulum (ER) stress and apoptosis in lung cancer cell H460 Wen-Yao Cui & Yan Liu & Yong-Qiang Zhu & Tao Song & Qiu-Shi Wang
Received: 18 November 2013 / Accepted: 22 January 2014 / Published online: 9 February 2014 # International Society of Oncology and BioMarkers (ISOBM) 2014
Abstract Propofol is one of the most commonly used intravenous anesthetic agents during cancer resection surgery. It can influence proliferation, motility, and invasiveness of cancer cells in vitro and in vivo. However, the role of the propofol in the lung cancer cells remains unclear. In this study, we demonstrated the effects of propofol on the proliferation and the apoptosis of lung cancer cell H460 by using colony formation assay and flow cytometry. Propofol also decreased tumor size and weight in established xenografted tumors. Furthermore, propofol-induced endoplasmic reticulum (ER) stress was determined by Western blot. Keywords Propofol . Lung cancer . Endoplasmic reticulum . Apoptosis . Caspase
influence proliferation, motility, and invasiveness of cancer cells in vitro and in vivo [6, 7]. Therefore, in this study, we investigated the possible antitumor properties of propofol in lung cancer cell H460 and the underlying mechanisms associated with its activity. Induction of the endoplasmic reticulum (ER) stress pathway known as the unfolded protein response (UPR) is activated in a number of disease processes such as obesity, diabetes, atherosclerosis, and cancer [8, 9]. In the present study, we examined the effect of propofol on lung cancer cells both in vivo and in vitro. We demonstrate that propofol induced apoptosis in H460 cells partly through ER stress.
Materials and methods H460 cell culture and drug exposure
Introduction Lung cancer continues to be the most commonly diagnosed cancer as well as the leading cause of cancer death in the world [1]. Surgery remains a primary treatment for lung cancer. However, the influence of the perioperative factors, such as anesthetic(s), on lung cancer cells was not clear [2]. Propofol (2, 6-diisopropylphenol) is one of the most commonly used intravenous anesthetic agents producing smooth induction and rapid recovery from anesthesia [3]. It produces a variety of pharmacodynamic effects, such as hypnosis to general anesthesia, relaxes amnestic and muscles, and downregulates the production of pro-inflammatory cytokines [4, 5]. Previous studies also showed that propofol can W.
