ArticleOncology letters2014
SKI-II reverses the chemoresistance of SGC7901/DDP gastric cancer cells.
Article in Oncology letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Targeting Sphingolipids for Cancer Therapy.Frontiers in oncology · 2021Review
- Hair Cell Loss Induced by Sphingosine and a Sphingosine Kinase Inhibitor in the Rat Cochlea.Neurotoxicity research · 2016Article
- Metformin Increases Sensitivity of Pancreatic Cancer Cells to Gemcitabine by Reducing CD133+ Cell Populations and Suppressing ERK/P70S6K Signaling.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cisplatin is frequently used in treating gastric cancers; however, acquired resistance to the drug often reduces the efficacy of therapy. The present study analyzed the efficacy of the combination of 4-[4-(4-chloro-phenyl)-thiazol-2-ylamino]-phenol (SKI-II) and cisplatin [cis-diamminedichloroplatinum (II); DDP] on the gastric cancer SGC7901/DDP cell line. The results revealed that SKI-II and DDP had a clear synergistic effect. Glutathione (GSH) and glutathione S-transferase (GST) levels decreased significantly subsequent to the cells being treated with the combination of DDP and SKI-II compared with the cells that were treated with DDP or SKI-II alone. Phosphorylated extracellular-signal-regulated kinase (p-ERK) and phosphorylated c-Jun N-terminal kinase (p-JNK) expression levels also decreased following treatment with SKI-II. The results suggested that SKI-II is able to reverse the drug resistance in human gastric carcinoma cells and enhance the antitumor effect of DDP through the ras/mitogen-activated protein kinase (MAPK) proliferation pathway.
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