ArticleMolecular medicine reports2017
Effects of salinomycin and 17‑AAG on proliferation of human gastric cancer cells in vitro.
Article in Molecular medicine reports, 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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9 authors at 1 institution in 1 country.
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Abstract
The aim of the present study was to investigate the effects and mechanisms of 17‑AAG combined with salinomycin treatment on proliferation and apoptosis of the SGC‑7901 gastric cancer cell line. An MTT assay was used to detect the proliferation of SGC‑7901 cells. Morphological alterations of cells were observed under inverted phase‑contrast and fluorescence microscopes. Cell cycle and apoptosis were assessed by flow cytometry analysis. The protein expression of nuclear factor (NF)‑κB p65 and Fas‑ligand (L) were evaluated by immunocytochemistry. Salinomycin with a concentration range of 1‑32 µmol/l was demonstrated to inhibit growth of SGC‑7901 cells effectively, affect the morphology and apoptosis rate of cells, and arrest SGC‑7901 cells in S phase. Furthermore, salinomycin significantly increased the protein expression of Fas‑L and decreased the protein expression of NF‑κB p65. The alterations in SGC‑7901 cells co‑treated with salinomycin and 17‑AAG were more significant compared with cells treated with one drug only. In conclusion, the individual use of salinomycin and combined use with 17‑AAG may significantly inhibit SGC‑7901 gastric cancer cell proliferation and induce cell apoptosis. The potential mechanisms may be associated with upregulation of Fas‑L and downregulation of NF‑κB. These results provide a basis for the potential use of salinomycin in gastric cancer treatment.
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