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Oncol Lett. 2018 Oct;16(4):4768-4772. doi: 10.3892/ol.2018.9162. Epub 2018 Jul 17.

Gefitinib induces non-small cell lung cancer H1650 cell apoptosis through downregulating tumor necrosis factor-related apoptosis-inducing ligand expression levels.

Author information

1
Department of Radiation Oncology, Yinzhou Affiliated Hospital to Medical School of Ningbo University, Ningbo, Zhejiang 315000, P.R. China.
2
Department of Central Laboratory, Yinzhou Affiliated Hospital to Medical School of Ningbo University, Ningbo, Zhejiang 315000, P.R. China.

Abstract

Non-small cell lung cancer (NSCLC) presents severe threats to the lives of patients. Gefitinib is one of the first-line drugs available for the treatment of NSCLC in the clinical setting. The present study investigated the effects of gefitinib on NSCLC H1650 cell viability and apoptosis via MTT assays and flow cytometry. Western blot analysis was employed to detect tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) expression levels in H1650 cells. In the present study, H1650 cells were treated with TRAIL siRNA or an empty plasmid vector control, followed by gefitinib treatment to investigate apoptosis. Gefitinib treatment markedly inhibited H1650 cell viability, induced apoptosis and reduced TRAIL expression levels. TRAIL interference enhanced H1650 cell apoptosis induced by gefitinib. TRAIL overexpression suppressed gefitinib-induced H1650 cell apoptosis. In addition, gefitinib induced NSCLC H1650 cell apoptosis by downregulating TRAIL expression levels.

KEYWORDS:

H1650 cell; apoptosis; gefitinib; tumor necrosis factor-related apoptosis-inducing ligand

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