Research Papers:

Identifying clinically relevant drug resistance genes in drug-induced resistant cancer cell lines and post-chemotherapy tissues

Mengsha Tong, Weicheng Zheng, Xingrong Lu, Lu Ao, Xiangyu Li, Qingzhou Guan, Hao Cai, Mengyao Li, Haidan Yan, You Guo, Pan Chi and Zheng Guo _

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Oncotarget. 2015; 6:41216-41227. https://doi.org/10.18632/oncotarget.5649

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Mengsha Tong1, Weicheng Zheng1, Xingrong Lu2, Lu Ao1, Xiangyu Li1, Qingzhou Guan1, Hao Cai1, Mengyao Li1, Haidan Yan1, You Guo1, Pan Chi2, Zheng Guo1

1Department of Bioinformatics, Key Laboratory of Ministry of Education for Gastrointestinal Cancer, Fujian Medical University, Fuzhou, China

2Department of Colorectal & Anal Surgery, Affiliated Union Hospital of Fujian Medical University, Fuzhou, China

Correspondence to:

Zheng Guo, e-mail: [email protected]

Pan Chi, e-mail: [email protected]

Keywords: drug-induced resistant cancer cell lines, drug treatment response, colorectal cancer, 5-fluorouracil, oxaliplatin

Received: June 30, 2015     Accepted: September 12, 2015     Published: October 15, 2015


Until recently, few molecular signatures of drug resistance identified in drug-induced resistant cancer cell models can be translated into clinical practice. Here, we defined differentially expressed genes (DEGs) between pre-chemotherapy colorectal cancer (CRC) tissue samples of non-responders and responders for 5-fluorouracil and oxaliplatin-based therapy as clinically relevant drug resistance genes (CRG5-FU/L-OHP). Taking CRG5-FU/L-OHP as reference, we evaluated the clinical relevance of several types of genes derived from HCT116 CRC cells with resistance to 5-fluorouracil and oxaliplatin, respectively. The results revealed that DEGs between parental and resistant cells, when both were treated with the corresponding drug for a certain time, were significantly consistent with the CRG5-FU/L-OHP as well as the DEGs between the post-chemotherapy CRC specimens of responders and non-responders. This study suggests a novel strategy to extract clinically relevant drug resistance genes from both drug-induced resistant cell models and post-chemotherapy cancer tissue specimens.

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