ArticleOncology letters2018
Tumor necrosis factor-related apoptosis-inducing ligand additive with Iodine-131 of inhibits non-small cell lung cancer cells through promoting apoptosis.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed, 6 citations in OpenAlex.
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-small-cell lung cancer (NSCLC) accounts for ~80% of human lung cancer cases and is the most common cause of cancer-associated mortality worldwide. Reports have indicated that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and Iodine-131 (I-131) can induce tumor cell apoptosis. The purpose of the present study was to investigate the additive efficacy of TRAIL and I-131 on NSCLC cells. The present study demonstrated that additive treatment of TRAIL and I-131 (TRAIL-I-131) significantly inhibited the growth and aggressiveness of NSCLC cells compared with single TRAIL or I-131 treatment. Results demonstrated that TRAIL-I-131 treatment induced apoptosis of NSCLC cells, with western blot analysis confirming that TRAIL-I-131 treatment increased proapoptotic Bad and Bax expression levels, while antiapoptotic Bcl-2 and Bcl-w protein levels were decreased in NSCLC cells. The present study demonstrated that TRAIL-I-131 treatment inhibited vascular endothelial growth factor (VEGF) and activator protein-1 (AP-1) in NSCLC cells. Potential mechanism analyses identified that TRAIL-I-131 treatment induced apoptosis of NSCLC cells through caspase-9 activation.
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