Establishment and characterization of irinotecan-resistant human non-small cell lung cancer A549 cells

Ikeda,Ryuji; Vermeulen,Lee C.; Lau,Elim; Jiang,Zhisheng; Pomplun,Marcia; Kolesar,Jill M.

doi:10.3892/mmr.2010.366

Establishment and characterization of irinotecan-resistant human non-small cell lung cancer A549 cells

Authors:
- Ryuji Ikeda
- Lee C. Vermeulen
- Elim Lau
- Zhisheng Jiang
- Marcia Pomplun
- Jill M. Kolesar
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Affiliations: Department of Clinical Pharmacy and Pharmacology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan, Division of Pharmacy Practice, School of Pharmacy, University of Wisconsin-Madison and Center for Drug Policy, University of Wisconsin Hospital and Clinics, Madison, WI, USA, School of Pharmacy, University of Wisconsin and University of Wisconsin Paul P. Carbone Comprehensive Cancer Center, Madison, WI, USA, School of Pharmacy, University of Wisconsin and University of Wisconsin Paul P. Carbone Comprehensive Cancer Center, 600 Highland Avenue, Room K4/554, Madison, 53705 WI, USA
Published online on: September 15, 2010 https://doi.org/10.3892/mmr.2010.366
Pages: 1031-1034

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Abstract

Irinotecan (CTP-11) is a topoisomerase I inhibitor used in the treatment of colorectal cancer and non-small cell lung cancer (NSCLC). Despite an initial response to therapy, resistance to irinotecan reduces its efficacy. We isolated irinotecan-resistant human NSCLC A549 cells, termed A549/CTP-11R cells. A549/CTP-11R cells were resistant to irinotecan, as well as paclitaxel, gemcitabine and carboplatin. Curcumin, a nuclear factor-κB (NF-κB) inhibitor, increased the sensitivity to irinotecan of A549/CTP-11R cells. The expression level of Bcl-XL and X-linked inhibitor of apoptosis protein, target genes of NF-κB, in A549/CTP-11R cells was higher than that in A549 cells. Our result suggests that the addition of curcumin to irinotecan reverses irinotecan resistance in NSCLC.