Published online Feb 21, 2017. doi: 10.3748/wjg.v23.i7.1189
Peer-review started: October 10, 2016
First decision: November 9, 2016
Revised: November 24, 2016
Accepted: December 16, 2016
Article in press: December 19, 2016
Published online: February 21, 2017
Processing time: 134 Days and 6.7 Hours
To explore novel therapeutic target of cisplatin resistance in human gastric cancer.
The sensitivity of SGC7901 cells and cisplatin-resistant SGC7901 cells (SGC7901/DDP) for cisplatin were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay. High-quality total RNA which isolated from SGC7901/DDP cells and SGC7901 cells were used for mRNA microarray analysis. Results were analyzed bioinformatically to predict their roles in the development of cisplatin resistance and the expression of 13 dysregulated mRNAs we selected were validated by quantitative real-time polymerase chain reaction (qRT-PCR).
SGC7901/DDP cells highly resistant to cisplatin demonstrated by MTT assay. A total of 1308 mRNAs (578 upregulated and 730 downregulated) were differentially expressed (fold change ≥ 2 and P-value < 0.05) in the SGC7901/DDP cells compared with SGC7901 cells. The expression of mRNAs detected by qRT-PCR were consistent with the microarray results. Gene Ontology, Kyoto Encyclopedia of Genes and Genomes pathway and protein-protein interaction analysis demonstrated that the differentially expressed mRNAs were enriched in PI3K-Akt, Notch, MAPK, ErbB, Jak-STAT, NF-kappaB signaling pathways which may be involved in cisplatin resistance. Several genes such as PDE3B, VEGFC, IGFBP3, TLR4, HIPK2 and EGF may associated with drug resistance of gastric cancer cells to cisplatin.
Exploration of those altered mRNAs may provide more promising strategy in diagnosis and therapy for gastric cancer with cisplatin resistance.
Core tip: We tested the sensitivity of human gastric cancer cells SGC7901/DDP and SGC7901 for cisplatin and compared their mRNA expression profile using a human mRNA microarray, and then performed bioinformatics analysis to depict comprehensively the properties of the differentially expressed mRNAs. Results demonstrated that the dysregulated mRNA were enriched in functions and pathways that may be involved in cisplatin resistance. Exploration of the dysregulated genes could suggest a promising strategy in diagnosis and therapy of gastric cancer with cisplatin resistance.