期刊
YONSEI MEDICAL JOURNAL
卷 57, 期 3, 页码 588-598出版社
YONSEI UNIV COLL MEDICINE
DOI: 10.3349/ymj.2016.57.3.588
关键词
Tolfenamic acid; nasopharyngeal cancer; p38 mitogen-activated protein kinase; Slug
资金
- Bio & Medical Technology Development Program [2012M3A9B2052870]
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Science, ICT and future Planning [2015R1A2A1A01002968]
- National Research Foundation of Korea [2015R1A2A1A01002968] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Purpose: Tolfenamic acid (TA), a non-steroidal anti-inflammatory drug, is known to exhibit antitumor effects in various cancers apart from nasopharyngeal cancer (NPC). NPC exhibits high invasiveness, as well as metastatic potential, and patients continue to suffer from residual, recurrent, or metastatic disease even after chemoradiation therapy. Therefore, new treatment strategies are needed for NPC. In this study, we investigated the efficacy and molecular mechanisms of TA in NPC treatment. Materials and Methods: TA-induced cell death was detected by cell viability assay in the NPC cell lines, HNE1 and HONE1. Wound healing assay, invasion assay, and Western blot analysis were used to evaluate the antitumor effects of TA in NPC cell lines. Results: Treatment with TA suppressed the migration and invasion of HNE1 and HONE1 cells. Hepatocyte growth factor enhanced the proliferation, migration, and invasion abilities of NPC cells. This enhancement was successfully inhibited by TA treatment. Treatment with TA increased phosphorylation of p38, and the inhibition of p38 with SB203580 reversed the cytotoxic, anti-invasive, and anti-migratory effects of TA treatment in NPC cell lines. Moreover, inhibition of p38 also reversed the decrease in expression of Slug that was induced by TA treatment. Conclusion: In conclusion, the activation of p38 plays a role in mediating TA-induced cytotoxicity and inhibition of invasion and migration via down-regulation of Slug.
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