Behaviors Of Nasopharyngeal Carcinoma Cells Research Articles

Sevoflurane inhibits the malignant behavior of nasopharyngeal carcinoma cells by regulating mitochondrial membrane potential.

This study aims to determine the effect of sevoflurane (Sev) on nasopharyngeal carcinoma (NPC) in malignant behavior and mitochondrial membrane potential (MMP). NPC cells (5-8F and CNE2) were exposed to Sev at different concentrations and then tested for proliferation by CCK-8 and colony formation assays, apoptosis by flow cytometry, and invasion and migration by Transwell assays. In addition, the Warburg effect was examined by measurements of glucose consumption, lactic acid production, and adenosine triphosphate (ATP). Mitochondrial function was evaluated by reactive oxygen species (ROS) production, oxidative stress-related indexes, and mitochondrial membrane potential. Sev suppressed 5-8F and CNE2 cell proliferation, invasion, and migration, and enhanced apoptosis. Moreover, Sev dampened the Warburg effect by reducing glucose consumption, lactic acid production, and ATP, as well as decreasing hexokinase 2 and pyruvate kinases type M2 protein expressions. Also, Sev induced ROS production and malondialdehyde content and reduced superoxide and glutathione peroxidase levels. Finally, Sev caused damage to mitochondrial homeostasis through induction of cleaved caspase-3, cleaved caspase-9, and cytochrome c protein expression and reduction of MMP. Sev inhibits the malignant behavior of NPC cells by regulating MMP.

Long Non-Coding RNA Cancer Susceptibility Candidate 9 Regulates the Malignant Biological Behavior of Nasopharyngeal Carcinoma Cells by Targeting miR-497-5p/Wnt3a/β-catenin Signaling Pathway.

Nasopharyngeal carcinoma (NPC) is a major kind of head and neck epithelial carcinoma. Increasing evidences reveal that long noncoding RNAs are considered as vital regulators in tumorigenesis and progression. Although previous studies have found that cancer susceptibility candidate 9 (CASC9) highly expresses in NPC, the underlying mechanisms need to be further studied. In this study, we found that CASC9 was overexpressed and associated with worse prognosis in NPC. CASC9 knockdown significantly inhibited the cell proliferation, migration and invasion in vitro and enhanced the sensitivity of tumor cells to cisplatin and paclitaxel. Mechanism research confirmed CASC9 regulated the malignant biological behavior of nasopharyngeal carcinoma cells by targeting miR-497-5p/Wnt3a/β-catenin signaling pathway. The present study might provide a novel mechanism for tumorigenesis and progression of NPC and contribute to the development of an effective molecular target therapy.

Long Noncoding RNA CRNDE Functions as an Oncogene to Facilitate Aggressive Behaviors of Nasopharyngeal Carcinoma Cells by Modulating miR-3163/TWIST1 Axis.

Long noncoding RNA (lncRNA) CRNDE has been broadly implicated in many malignancies. The aim of this study was to explore the function and potential mechanisms of CRNDE in nasopharyngeal carcinoma (NPC). Here, we discovered that CRNDE level was increased in NPC tissues and cell lines. Additionally, elevated CRNDE positively correlated with large tumor size, advanced TNM stage, distant metastasis, EBV infection and worse prognosis. Furthermore, depletion of CRNDE significantly impaired the capacity of proliferation, migration and invasion in NPC cells. Mechanically, CRNDE could serve as a molecular sponge of miR-3163 to regulate the expression of TWIST1. Importantly, the inhibitory effects of CRNDE knockdown on cell proliferation and metastasis were blocked by silence of miR-3163 or restoration of TWIST1 expression. Overall, our data highlighted that CRNDE could promote NPC progression via altering miR-3163/TWIST1 axis, suggesting CRNDE as a potential prognostic biomarker and therapeutic target for NPC treatment.

Long noncoding RNA ANCR promotes migration, invasion, EMT progress and stemness of nasopharyngeal carcinoma cells via the miR-4731-5p/NMT1 axis

BackgroundIn our previous study, we revealed that Antidifferentiation noncoding RNA (ANCR) promoted proliferation and radiation resistance of nasopharyngeal carcinoma (NPC) cells. However, the molecular mechanism and function of ANCR are not fully studied. The current study aimed to further investigate the role and underlying molecular mechanism of ANCR in NPC. MethodsRT-qPCR and western blot analyses were used to detect the levels of RNAs and proteins in NPC cells. Wound healing and Transwell assays were used to examine the migration and invasion of NPC cells. The relationship among ANCR, miR-4731-5p and N-myristoyltransferase 1 (NMT1) was investigated by RIP and luciferase reporter assays. The NPC cell stemness was accessed by the sphere formation assay. ResultsANCR was significantly highly expressed in NPC cell lines. Silenced ANCR suppressed cell migration, invasion epithelial-mesenchymal transition (EMT) process and cell stemness in NPC. Furthermore, ANCR sponged miR-4731-5p to upregulate the NMT1 expression. Rescue assays indicated that NMT1 neutralized the antioncogenic effect induced by silenced ANCR on NPC cells. ConclusionsLong noncoding RNA ANCR suppresses malignant behaviors of nasopharyngeal carcinoma cells by regulating miR-4731-5p/NMT1 axis.

In vitro study of joint intervention of E-cad and Bmi-1 mediated by transcription activator-like effector nuclease in nasopharyngeal carcinoma

To explore the effect of intervention of E-cadherin (E-cad) and B-lymphoma Moloney murine leukemia virus insertion region-1 (Bmi-1) mediated by transcription activator-like effector nuclease (TALEN) on the biological behaviors of nasopharyngeal carcinoma cells. Methods: Multi-locus gene targeting vectors pUC-DS1-CMV-E-cad-2A-Neo-DS2 and pUC-DS1-Bmi-1 shRNA-Zeo-DS2 were constructed, and the E-cad and Bmi-1 targeting vectors were transferred with TALEN plasmids to CNE-2 cells individually or simultaneously. The integration of target genes were detected by PCR, the expressions of E-cad and Bmi-1 were detected by Western blot. The changes of cell proliferation were detected by cell counting kit-8 (CCK-8) assay. The cell cycle and apoptosis were detected by flow cytometry. The cell migration and invasion were detected by Transwell assay. Results: The E-cad and Bmi-1 shRNA expression elements were successfully integrated into the genome of CNE-2 cells, the protein expression level of E-cad was up-regulated, and the protein expression level of Bmi-1 was down-regulated. The intervention of E-cad and Bmi-1 didn't affect the proliferation, cell cycle and apoptosis of CNE-2 cells, but it significantly inhibited the migration and invasion ability of CNE-2 cells. Furthermore, the intervention of E-cad and Bmi-1 together significantly inhibited the migration ability of nasopharyngeal carcinoma cells compared with the intervention of E-cad or Bmi-1 alone (all P<0.01). Conclusion: The joint intervention of E-cad and Bmi-1 mediated by TALEN can effectively inhibit the migration and invasion of nasopharyngeal carcinoma cells in vitro, which may lay the preliminary experimental basis for gene therapy of human cancer.

The inhibitory effects of extracellular ATP on the growth of nasopharyngeal carcinoma cells via P2Y2 receptor and osteopontin.

BackgroundNasopharyngeal carcinoma (NPC) is a common malignant tumor observed in the populations of southern China and Southeast Asia. However, little is known about the effects of purinergic signal on the behavior of NPC cells. This study analyzed the effects of ATP on the growth and migration of NPC cells, and further investigated the potential mechanisms during the effects.MethodsCell viability was estimated by MTT assay. Transwell assay was utilized to assess the motility of NPC cells. Cell cycle and apoptosis were detected by flow cytometry analysis. Changes in OPN, P2Y2 and p65 expression were assessed by western blotting analysis or immunofluorescence. The effects of ATP and P2Y2 on promoter activity of OPN were analyzed by luciferase activity assay. The binding of p65 to the promoter region of OPN was examined by ChIP assay.ResultsAn MTT assay indicated that ATP inhibited the proliferation of NPC cells in time- and dose-dependent manners, and a Transwell assay showed that extracellular ATP inhibited the motility of NPC cells. We further investigated the potential mechanisms involved in the inhibitory effect of extracellular ATP on the growth of NPC cells and found that extracellular ATP could reduce Bcl-2 and p-AKT levels while elevating Bax and cleaved caspase-3 levels in NPC cells. Decreased levels of p65 and osteopontin were also detected in the ATP-treated NPC cells. We demonstrated that extracellular ATP inhibited the growth of NPC cells via p65 and osteopontin and verified that P2Y2 overexpression elevated the inhibitory effect of extracellular ATP on the proliferation of NPC cells. Moreover, a dual luciferase reporter assay showed that the level of osteopontin transcription was inhibited by extracellular ATP and P2Y2. ATP decreased the binding of p65 to potential sites in the OPN promoter region in NPC cells.ConclusionThis study indicated that extracellular ATP inhibited the growth of NPC cells via P2Y2, p65 and OPN. ATP could be a promising agent serving as an adjuvant in the treatment of NPC.