Analgecine enhances the anti-tumor response of radiotherapy by increasing apoptosis and cell cycle arrest in non-small cell lung cancer
PDF | HTML | Supplementary Files | How to cite
Metrics: PDF 1253 views | HTML 2072 views | ?
Xue Chen1, Xibing Zhuang1, Qi Zhang1, Youjun Luo1, Sujuan Yuan1 and Tiankui Qiao1
1Department of Oncology, Jinshan Hospital, Medical Center of Fudan University, Jinshan District, Shanghai 201500, People’s Republic of China
Tiankui Qiao, email: [email protected]
Keywords: analgecine, apoptosis, cell cycle, non-small cell lung cancer, radiotherapy
Received: October 13, 2016 Accepted: July 11, 2017 Published: August 7, 2017
We investigated whether Analgecine treatment enhanced the antitumor response of radiotherapy in non-small cell lung cancer (NSCLC) cells. Lewis lung carcinoma (LLC) xenograft mice treated with Analgecine plus irradiation showed reduced tumor growth and increased survival. Tumor cell apoptosis was enhanced by Analgecine, based on TUNEL assays. It also increased plasma levels of pro-inflammatory cytokines (IL-6, IL-12, and IFN-γ) and decreased anti-inflammatory cytokines (TGFβ and IL-10), suggesting an enhanced immune response. Analgecine plus irradiation reduced cell viability and colony formation by A549 NSCLC cells. Analgecine treatments also activated apoptotic signaling with increased levels of pro-apoptotic proteins, including cytochrome c, caspase-3, cleaved caspase-3, caspase-9, p53 and Bax, and decreased Bcl2. Analgecine enhanced G2/M phase arrest in A549 cells by decreasing cyclinB1 and CDK1. These observations demonstrate that Analgecine combined with radiotherapy enhances anti-tumor responses by inducing apoptosis and cell cycle arrest. Moreover, they suggest possible future clinical application of Analgecine for the treatment of NSCLC.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.