| Literature DB >> 27108960 |
Ying Wu1, Dan-Dan Yu1, Yong Hu2, Dali Yan2, Xiu Chen2, Hai-Xia Cao3, Shao-Rong Yu3, Zhuo Wang3, Ji-Feng Feng2.
Abstract
Mutations in the epidermal growth factor receptor (EGFR) make lung adenocarcinoma cells sensitive to EGFR tyrosine kinase inhibitors (TKIs). Long-term cancer therapy may cause the occurrence of acquired resistance to EGFR TKIs. Long non-coding RNAs (lncRNAs) play important roles in tumor formation, tumor metastasis and the development of EGFR-TKI resistance in lung cancer. To gain insight into the molecular mechanisms of EGFR-TKI resistance, we generated an EGFR-TKI-resistant HCC827-8-1 cell line and analyzed expression patterns by lncRNA microarray and compared it with its parental HCC827 cell line. A total of 1,476 lncRNA transcripts and 1,026 mRNA transcripts were dysregulated in the HCC827‑8-1 cells. The expression levels of 7 chosen lncRNAs were validated by real-time quantitative PCR. As indicated by functional analysis, several groups of lncRNAs may be involved in the bio-pathways associated with EGFR-TKI resistance through their cis- and/or trans‑regulation of protein-coding genes. Thus, lncRNAs may be used as novel candidate biomarkers and potential targets in EGFR-TKI therapy in the future.Entities:
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Year: 2016 PMID: 27108960 DOI: 10.3892/or.2016.4758
Source DB: PubMed Journal: Oncol Rep ISSN: 1021-335X Impact factor: 3.906