Effects of Arctigenin in Proliferation, Migration, and Invasion of Nasopharyngeal Carcinoma 5-8F Cells

Author(s):

Dongdong Huang, Rui Lu, Mingjing Cai, Jie Meng, Shuangba He, Qingxiang Zhang and Wei Meng*   Pages 1211 - 1216 ( 6 )

Abstract:

<p> Background: Nasopharyngeal carcinoma (NPC) is a malignant tumor of the nasopharynx. </p><p> Objective: Here, we aimed to understand better the molecular basis for arctigenin (ARG)’s ability to promote NPC 5- 8F cell invasion. </p><p> Methods: We tested the effects of several doses of ARG on 5-8F cells that had been cultured in vitro. We estimated the metabolic activity of cells by The MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) tetrazolium assay. We examined the influence on cell invasion, and migration using Transwell Evaluation. Real-time polymerase chain reaction analysis was used to determine the relative amounts of epidermal growth factor receptor (EGFR), Janus kinase 2 (JAK2) , and transcriptional activator 3 (STAT 3) mRNA expression. Using western blotting, we looked at the level of phosphorylation of specific proteins like EGFR, phosphorylated EGFR, JAK2, and STAT 3. </p><p> Results: Our findings revealed that ARG inhibited NPC 5-8F cell development in a dose-and time-dependent manner. The invasiveness and mobility of 5-8F cells were significantly suppressed when ARG was overexpressed in a tumor development model. Expression levels of EGFR, JAK2, and STAT 3 mRNA were considerably low in the experimental group. As a consequence of being treated with ARG, lower levels of EGFR, p-EGFR, p-JAK2, and p-STAT3 expression were observed. </p><p> Conclusion: These results suggest that ARG may prevent NPC 5-8F cells from proliferating, migrating, and invading other tissues. There are a few potential molecular pathways, two of which are the inhibition of EGFR phosphorylation and the reduction of levels of phospho-JAK2 and phospho-STAT3.</p>

Keywords:

Arctigenin , nasopharyngeal carcinoma, migration, invasion, proliferation, western blotting.

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