This study examined four human cancer cell lines including A549 (lung adenocarcinoma), U251MG (glioma), Tca8113 (tongue squamous carcinoma), and CNE-2 (nasopharyngeal carcinoma).
Then, Western blotting and quantitative real-time PCR (qPCR) were performed to examine TLN1 levels, and qPCR was used to determine miR-429 levels in NPC cell lines with different metastatic characteristics (5-8F, CNE-2, CNE-1, 6-10B and NP69), to investigate whether TLN1 and miR-429 are correlated with the metastatic characteristics of these cells.
<b>Objective:</b> The purpose of our study is to investigate the role of miR-17-5p in angiogenesis of nasopharyngeal carcinoma and the crosstalk between HUVECs and CNE-2 via exosomes.
Seventy-two nude mice were implanted with CNE-1 (low radio-sensitive) and CNE-2 (high radio-sensitive) NPC cell lines, and their respective xenografts were obtained.
Evofosfamide exhibited hypoxia-selective cytotoxicity in NPC cell lines, with 50% inhibition concentration (IC<sub>50</sub>) values of 8.33 ± 0.75, 7.62 ± 0.67, and 0.31 ± 0.07 μmol/L under hypoxia in CNE-2, HONE-1 and HNE-1 cells, respectively.
To investigate the antitumour efficacy of pachymic acid (PA), which is a fungal extract component, on nasopharyngeal carcinoma (NPC) cells CNE-1, CNE-2.
CD133- cells were obtained from human nasopharyngeal carcinoma cells (CNE-1 and CNE-2) based on CD133-labeled fluorescence-activated cell sorting (FACS) and magnetic-activated cell sorting (MACS), respectively.
The purpose of this study was to determine the effect and mechanism by which 2-ME2 inhibits nasopharyngeal carcinomaCNE-2 stem-like cell (NPCSC) proliferation and migration and reduces NPCSC radioresistance.
We identified that its target gene Rab27B negatively correlates with miR-20a-5p-mediated NPC radio-resistance by systematic studies of a radio-sensitive (CNE-2) and resistant (CNE-1) NPC cell lines.
In this study, we evaluated whether morphine modulates cisplatin-induced apoptosis in human nasopharyngeal carcinoma CNE-2 cells and whether morphine affects the antitumor activity of cisplatin on tumor growth in human nasopharyngeal carcinomaCNE-2 xenografts in nude mice.
We examined the function of survivin gene expression in patients with nasopharyngeal carcinoma (NPC), as well as small interfering RNA (siRNA) on controlling CNE-2NPC proliferation and apoptosis.
This study investigated the effect of sodium selenite (Na2SeO3) on proliferation, cell cycle, apoptosis as well as the underlying mechanism in CNE-2nasopharyngeal carcinoma (NPC) cells.
PARP-1 promotes autophagy via the AMPK/mTOR pathway in CNE-2 human nasopharyngeal carcinoma cells following ionizing radiation, while inhibition of autophagy contributes to the radiation sensitization of CNE-2 cells.
Additionally, flow cytometric and analysis electron microscopy revealed the inhibition of cell cycle progression and reduction of apoptosis, respectively, in human NPC cell lines including CNE-1 and CNE-2 in vitro.
In vitro experiments further showed that WIP1 inhibition led to a decrease in the proliferative ability of NPCCNE-2 and 5-8F cells accompanied by cell cycle arrest and increased apoptosis.
CNE-2, a highly metastatic human NPC cell line in which HPSE mRNA and protein levels were detected to be the highest in three NPC cell lines involved in the research, was selected as a cell model in vitro and in vivo.
Then, functional and mechanical analyses of miRNA-324-3p in NPC radioresistance were performed by overexpression and down-regulation of miRNA-324-3p in CNE-2-Rs cells and its parental cells.
In this study, CNE-2 was found to be the most resistant NPC cell line to TRAIL, and whether Bcl-2 small-interfering RNA (siRNA) and phosphatidylinositol 3-kinase (PI3-K) inhibitors (LY294002 and Wortmannin) could prevent TRAIL resistance in CNE-2 was also investigated.
The present study employed 5-aza-2'-deoxycytidine (5-aza-CdR) to treat nasopharyngeal carcinoma cell line CNE-1, CNE-2 and non-cancerous human nasopharyngeal epithelial cell line NP-69 to understand the effects on spleen tyrosine kinase (Syk) gene promoter methylation.