| Literature DB >> 29118912 |
Jinting Wang1, Lian Deng1, Junpeng Huang2, Rui Cai1, Xiongjie Zhu1, Faquan Liu3, Qien Wang4, Jiren Zhang1, Yanfang Zheng1.
Abstract
Fibronectin 1 (FN1) is a member of the glycoprotein family located on chromosome 2q35. It has been reported that FN1 is upregulated in many tumors, and its expression is negatively related to the prognosis and survival of cancer patients. Through data analysis, we found that FN1 is upregulated in nasopharyngeal carcinoma (NPC). This study aimed to investigate how FN1 expression affects NPC cell behavior. In this study, we downregulated FN1 in two NPC cell lines, 5-8F (EBV-) and C666-1 (EBV+), and evaluated invasion, migration and apoptosis. FN1 promoted migration and invasion by upregulating MMP9 and MMP2 expression; the NF-κB/P65 signaling pathway was also affected by FN1. FN1 suppressed apoptosis in NPC cells by upregulating BCL2 and increasing the nuclear localization of P65, both by inducing cytosolic accumulation and nuclear translocation, but FN1 expression was not reduced when the NF-κB/P65 pathway was inhibited in the negative control (NC) group. Compared with NC cells, shFN1 cells showed little change in apoptosis when the NF-κB/P65 pathway was activated by LPS. These results suggest that FN1 regulates apoptosis though P65 in the NF-κB pathway. Our results show that FN1 plays an important role in NPC cells and is a potential target for NPC treatment.Entities:
Keywords: Fibronectin 1; NF-κB/P65 pathway; Nasopharyngeal carcinoma; apoptosis
Year: 2017 PMID: 29118912 PMCID: PMC5666059
Source DB: PubMed Journal: Am J Transl Res Impact factor: 4.060