Abstract:
:Gefitinib, an epidermal growth factor receptor tyrosine kinase inhibitor, has been frequently used in targeted therapy for lung cancer. However, the widespread use of gefitinib in targeted therapy for patients with lung cancer is hampered by its common skin toxicities. The present study aimed to investigate the mechanisms underlying the skin toxicities of gefitinib. Normal human epidermal keratinocytes (NHEKs) treated with gefitinib were used for a series of in vitro assays, including MTT, reverse transcription‑quantitative polymerase chain reaction, western blot analysis, immunohistochemistry and transepithelial electrical resistance and paracellular permeability detection. In the present study, it was determined that the skin toxicities of gefitinib may be due to claudin (CLDN)1 and CLDN4 downregulation and CLDN2 upregulation in NHEKs. Additionally, Src and signal transducer and activator of transcription 3 pathways were involved in gefitinib‑induced barrier function disruption in NHEKs. In conclusion, the present study may provide novel insights for improving skin toxicity of gefitinib in patients with lung cancer.
journal_name
Int J Mol Medjournal_title
International journal of molecular medicineauthors
Fang H,Wang Y,Xu L,Zhou S,Bai J,Wu Y,Qiao J,Jiang X,Zhu D,Ding Ydoi
10.3892/ijmm.2018.4046subject
Has Abstractpub_date
2019-03-01 00:00:00pages
1522-1530issue
3eissn
1107-3756issn
1791-244Xjournal_volume
43pub_type
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