ArticleThe Journal of biological chemistry2009
Identification of GAS1 as an epirubicin resistance-related gene in human gastric cancer cells with a partially randomized small interfering RNA library.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 43 citations in OpenAlex.
- Multidrug Resistance in Cancer: Understanding Molecular Mechanisms, Immunoprevention and Therapeutic Approaches.Frontiers in oncology · 2022Review
- Heat Shock Protein 90 Triggers Multi-Drug Resistance of Ovarian Cancer via AKT/GSK3β/β-Catenin Signaling.Frontiers in oncology · 2021Article
- Article
- microRNA-mediatedExperimental and therapeutic medicine · 2019Article
- Transcriptional upregulation of c-MYC by AXL confers epirubicin resistance in esophageal adenocarcinoma.Molecular oncology · 2018Article
- AlPcSInternational journal of nanomedicine · 2018Article
- RNF138 confers cisplatin resistance in gastric cancer cells via activating Chk1 signaling pathway.Cancer biology & therapy · 2018Article
- HNF-4α promotes multidrug resistance of gastric cancer cells through the modulation of cell apoptosis.Oncology letters · 2017Article
- shRNA target prediction informed by comprehensive enquiry (SPICE): a supporting system for high-throughput screening of shRNA library.EURASIP journal on bioinformatics & systems biology · 2016Article
- ABCG2 inhibition as a therapeutic approach for overcoming multidrug resistance in cancer.Journal of biosciences · 2016Review
- Biased random walk model for the prioritization of drug resistance associated proteins.Scientific reports · 2015Article
- miR-508-5p regulates multidrug resistance of gastric cancer by targeting ABCB1 and ZNRD1.Oncogene · 2014Article
- Integrated analysis of DNA methylation and mRNA expression profiling reveals candidate genes associated with cisplatin resistance in non-small cell lung cancer.Epigenetics · 2014Article
- HDM2 regulation by AURKA promotes cell survival in gastric cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- Transcription factor CUTL1 is a negative regulator of drug resistance in gastric cancer.The Journal of biological chemistry · 2013Article
- Role of breast cancer resistance protein (BCRP/ABCG2) in cancer drug resistance.Biochemical pharmacology · 2012Review
- Lentiviral transfer of an inducible transgene expressing a soluble form of Gas1 causes glioma cell arrest, apoptosis and inhibits tumor growth.Cancer gene therapy · 2011Article
- Article
- Functional toxicogenomics: mechanism-centered toxicology.International journal of molecular sciences · 2010Review
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epirubicin has been widely used for chemotherapeutic treatment of gastric cancer; however, intrinsic and acquired chemoresistance remains an obstacle to successful management. The mechanisms underlying epirubicin resistance are still not well defined. Here we report the construction and application of a partially randomized retrovirus library of 4 x 10(6) small interfering RNAs to identify novel genes whose suppression confers epirubicin resistance in gastric cancer cells SGC7901. From 12 resistant cell colonies, two small interfering RNAs targeting GAS1 (growth arrest-specific 1) and PTEN (phosphatase and tensin homolog), respectively, were identified and validated. We identified a previously unrecognized chemoresistance role for GAS1. GAS1 suppression resulted in significant epirubicin resistance and cross-resistance to 5-fluorouracil and cisplatin in various gastric cancer cell lines. GAS1 suppression promoted multidrug resistance through apoptosis inhibition, partially by up-regulating the Bcl-2/Bax ratio that was abolished by Bcl-2 inhibition. GAS1 suppression induced chemoresistance partially by increasing drug efflux in an ATP-binding cassette transporter and drug-dependent manner. P-glycoprotein (P-gp) and BCRP (breast cancer resistance protein) but not MRP-1 were up-regulated, and targeted knockdown of P-gp and BCRP could partially reverse GAS1 suppression-induced epirubicin resistance. Verapamil, a P-gp inhibitor, could reverse P-gp substrate (epirubicin) but not non-P-gp substrate (5-fluorouracil and cisplatin) resistance in GAS1-suppressed gastric cancer cells. BCRP down-regulation could partially reverse 5-fluorouracil but not cisplatin resistance induced by GAS1 suppression, suggesting 5-fluorouracil but not cisplatin was a BCRP substrate. These results suggest that GAS1 might be a target to overcome multidrug resistance and provide a novel approach to identifying candidate genes that suppress chemoresistance of gastric cancers.
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