ArticleOncotarget2017
Analgecine enhances the anti-tumor response of radiotherapy by increasing apoptosis and cell cycle arrest in non-small cell lung cancer.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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6 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
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.
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