ArticleCancer science2006
Role of ABCG2 as a biomarker for predicting resistance to CPT-11/SN-38 in lung cancer.
Article in Cancer science, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 43 citations in OpenAlex.
- Repressing PDCD4 activates JNK/ABCG2 pathway to induce chemoresistance to fluorouracil in colorectal cancer cells.Annals of translational medicine · 2021Article
- Pyrotinib Sensitizes 5-Fluorouracil-Resistant HER2Oncology research · 2020Article
- Establishment and Characterization of a Topotecan Resistant Non-small Cell Lung Cancer NCI-H460/TPT10 Cell Line.Frontiers in cell and developmental biology · 2020Article
- Synthesis of novel 10,11-methylenedioxy-camptothecin glycoside derivatives and investigation of their anti-tumor effectsRSC advances · 2019Article
- PharmGKB summary: very important pharmacogene information for ABCG2.Pharmacogenetics and genomics · 2017Review
- Molecular characterization of irinotecan (SN-38) resistant human breast cancer cell lines.BMC cancer · 2016Article
- FL118, a novel camptothecin analogue, overcomes irinotecan and topotecan resistance in human tumor xenograft models.American journal of translational research · 2015Article
- Genetic variation: effect on prostate cancer.Biochimica et biophysica acta · 2014Review
- Molecular mechanisms contributing to resistance to tyrosine kinase-targeted therapy for non-small cell lung cancer.Cancer biology & medicine · 2012Article
- Overexpression of carboxylesterase-2 results in enhanced efficacy of topoisomerase I inhibitor, irinotecan (CPT-11), for multiple myeloma.Cancer science · 2008Article
- Antipsychotic drugs inhibit the function of breast cancer resistance protein.Basic & clinical pharmacology & toxicology · 2008Article
- Recent advances on the molecular mechanisms involved in the drug resistance of cancer cells and novel targeting therapies.Clinical pharmacology and therapeutics · 2008Review
- Multiple drugbinding sites on the R482G isoform of the ABCG2 transporter.British journal of pharmacology · 2006Article
- Contribution of tumoral and host solute carriers to clinical drug response.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapyReview
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To examine the mechanism of resistance to 7-ethyl-10-hydroxycamptothecin (SN-38) in lung cancer, we continuously exposed the non-small-cell lung cancer (NSCLC) cell line NCI-H23 to SN-38 and selected the SN-38-resistant clone H23/SN-38. After 2 months of culturing in SN-38-free conditions, H23/SN-38 cells recovered their sensitivity to SN-38 and were subsequently established as the revertant H23/SN-38REV cell line. Because H23/SN-38 cells show cross resistance to certain anticancer drugs, such as topotecan, etoposide, doxorubicin and mitoxantrone, we examined the gene and protein expression levels of drug efflux transporters of the ATP-binding cassette (ABC) family. We found that both gene and protein expression of ABCG2/BCRP (ABCG2) in H23/SN-38 cells was increased compared with that in NCI-H23 cells and H23/SN-38REV cells. The cellular accumulation of topotecan in H23/SN-38 cells was decreased compared with that in NCI-H23 and H23/SN-38REV cells, and treatment with reserpine (an inhibitor of ABCG2) increased the cellular accumulation of topotecan in H23/SN-38 cells. Furthermore, treatment with reserpine also altered the sensitivity of H23/SN-38 cells to SN-38. These results indicate that the upregulation of ABCG2 was functional, and related to the resistance of H23/SN-38 cells to SN-38. Moreover, we found that gene expression levels of ABCG2 were significantly correlated with the concentration of SN-38 for 50% cell survival in 13 NSCLC cells (r=0.592, P<0.05). The present results indicate that the induction of ABCG2 by SN-38 does confer acquired resistance to CPT-11/SN-38, but the induction of ABCG2 and subsequent drug resistance are reversible. However, the expression level of ABCG2 may be a useful indicator of CPT-11/SN-38 activity in lung cancer.
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