MiR-100 inhibits invasion and migration of nasopharyngeal carcinoma cells by regulating ZBTB7A gene

2018 ◽  
Vol 29 (2) ◽  
Author(s):  
Yi Gang Zhao ◽  
Xian Zhi Wang
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Carcinoma Cells ◽  
Invasion And Migration ◽  
And Migration

scholarly journals Long noncoding RNA UCA1 promotes the proliferation, invasion, and migration of nasopharyngeal carcinoma cells via modulation of miR-145

2018 ◽  
Vol Volume 11 ◽  
pp. 7483-7492 ◽  
Author(s):  
Jing Wu ◽  
Mingyu Du ◽  
Qian Zhang ◽  
Wenjun Zhang ◽  
Yanxin Fan ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Carcinoma Cells ◽  
Invasion And Migration ◽  
And Migration

scholarly journals Indole-thiazolidinone conjugate inhibits nasopharyngeal carcinoma cell migration and invasion by targeting NF κB pathway

2021 ◽  
Vol 18 (3) ◽  
pp. 519-525
Author(s):  
Guoping Zhang ◽  
Sheng Zhang
Keyword(s):  
Cell Proliferation ◽  
Nasopharyngeal Carcinoma ◽  
Matrix Metalloproteinase ◽  
Carcinoma Cells ◽  
Matrix Metalloproteinase 2 ◽  
Migration And Invasion ◽  
Nuclear Fraction ◽  
Invasion And Migration ◽  
Migration Potential ◽  
And Migration

Purpose: To investigate the effect of indole-thiazolidinone on metastasis in HK1 nasopharyngeal carcinoma cells. Methods: HK1 cell proliferation was determined colorimetrically using 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay. Invasion and migration of HK1 cells were assessed using Matrigel™ chamber coated invasion and wound healing assays, respectively. Results: Indole-thiazolidinone suppressed proliferation of HK1 and NPC 039 NPC cell lines at 72 h. The degree of proliferation of HK1 cells on treatment with 0.25, 0.5, 1.0, 1.5, 2.0, 2.5 and 3.0 μM indolethiazolidinone was 99, 87, 71, 64, 49, 38 and 31 %, respectively. In HK1 cell cultures, migration potential was reduced to 58.32, 47.54, 28.91 and 17.65 %, on exposure to 1.5, 2.0, 2.5 and 3.0 μM indole-thiazolidinone, respectively. Incubation with 1.5, 2.0, 2.5 and 3.0 μM indole-thiazolidinone resulted in cell invasion values of 63.41, 49.37, 35.12 and 19.67 %, respectively. There was a marked decrease in the expressions of matrix metalloproteinase 2 and matrix metalloproteinase 9 in HK1 cells on treatment with indole-thiazolidinone (p < 0.05). In addition, indole-thiazolidinone treatment resulted in decrease in p65 and p50 in nuclear fraction. Treatment of HK1 and NPC 039 cells with indolethiazolidinone and henenalin synergistically decreased cell proliferation. Indole-thiazolidinone treatment caused significant decrease in tumor growth in mice (p < 0.05). Conclusion: Indole-thiazolidinone inhibits proliferation and metastasis in nasopharyngeal carcinoma cells. Therefore, it has potential for development as a therapeutic management of nasopharyngeal carcinoma in humans.

MiR-145, a microRNA targeting ADAM17, inhibits the invasion and migration of nasopharyngeal carcinoma cells

2015 ◽  
Vol 338 (2) ◽  
pp. 232-238 ◽  
Author(s):  
Jing Wu ◽  
Li Yin ◽  
Ning Jiang ◽  
Wen-jie Guo ◽  
Jia-jia Gu ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Carcinoma Cells ◽  
Invasion And Migration ◽  
And Migration

scholarly journals ResolvinD1 attenuates high-mobility group box 1-induced epithelial-to-mesenchymal transition in nasopharyngeal carcinoma cells

2019 ◽  
Vol 244 (18) ◽  
pp. 1608-1618
Author(s):  
Pingli Yang ◽  
Shan Chen ◽  
Gang Zhong ◽  
Yan Wang ◽  
Weijia Kong ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Gene Silencing ◽  
Epithelial To Mesenchymal Transition ◽  
High Mobility ◽  
Carcinoma Cells ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration ◽  
Emt Markers

Epithelial-to-mesenchymal transition (EMT) process is prevalent during the progression of tumors. Nasopharyngeal carcinoma (NPC) is no exception. High-mobility group box 1 (HMGB1) was reported to have the effect of inducing EMT in malignancy. However, the impact of HMGB1-induced EMT in NPC is unclear. Resolvin D1 (RvD1) was reported to regress the progression of inflammation and apoptosis of phagocytes. The effect of RvD1 in the EMT is largely unknown. The current research explored the role of RvD1 on HMGB1-induced EMT in NPC. EMT markers were investigated in 10 NPC and 10 nasopharyngitis (NPG) patients using immunohistochemistry and Western blot. In vitro, expression of EMT markers and HMGB1 in CNE1 and CNE2 cells was assessed with immunohistochemical, Western blot, and confocal microscopy after treatment with recombinant human HMGB1 (rhHMGB1) or HMGB1 gene silencing or RvD1. The invasion and migration of NPC cells were detected by scratch test and transwell assay. Overexpression and gene silencing of lipoxin A4 receptor/formyl peptide receptor 2 (ALX/FPR2) and G protein-coupled receptor 32 (GPR32) in CNE2 cells confirmed the effect of RvD1 using Western blots. N-cadherin, vimentin, and HMGB1 were found up-regulated in NPC samples compared with NPG samples, while ZO-1 and E-cadherin were down-regulated in NPC tissues. RhHMGB1-induced EMT in CNE1 and CNE2 cells in a dose-dependent way. CNE2 cell lines treated with rhHMGB1 possessed greater invasion and migration ability, which was confirmed by gene silencing. RvD1 suppressed HMGB1-induced EMT in NPC cells via ALX/FPR2 and GPR32 receptors. These results showed that EMT was obvious in NPC. HMGB1 played a key role in inducing EMT. RvD1 inhibited HMGB1-induced EMT and might have potential application in the area of NPC treatment. Impact statement Nasopharyngeal carcinoma has a high incidence in China. Discussing the molecular mechanism of nasopharyngeal carcinoma is important because of high recurrent rate and low quality of life after treatment. HMGB1, as an important inflammatory factor, promotes the process in many cancers. But little is known about how HMGB1 affects the progress of nasopharyngeal carcinoma cells. In our research, we assessed the role of HMGB1 on metastasis and invasion of nasopharyngeal carcinoma cells. The result of study indicates HMGB1-induced EMT in nasopharyngeal carcinoma cells. Furthermore, we observed that RvD1, which plays an actively protective role in many diseases, controls the migration and invasion of nasopharyngeal carcinoma cells by inhibiting the HMGB1-induced EMT. RvD1 can be further studied as a protective factor for nasopharyngeal carcinoma.

Study on the Mechanism of Long Non-Coding RNA-An Antisense Transcript of SATB Homeobox 2 in Promoting the Growth, Invasion and Migration of Nasopharyngeal Carcinoma

2021 ◽  
Vol 11 (1) ◽  
pp. 99-105
Author(s):  
Hualong Qiang ◽  
Shiyin Ma ◽  
Xiaodong Zhan ◽  
Chengyi Jiang ◽  
Yuefeng Han ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Carcinoma Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Luciferase Reporter Gene ◽  
Invasion And Migration ◽  
Potential Marker ◽  
Non Coding Rna ◽  
Gene Test ◽  
And Migration

This study intends to clarify lncRNA SATB2-AS1’s role in growth, invasion and migration of nasopharyngeal carcinoma cells and its effect on radiotherapy. The lncRNA array was used to analyze the differential expression of lncRNA in nasopharyngeal carcinoma biopsy tissues. QRT-PCR measured the levels of SATB2-AS1 and TIMP2 along with analysis of cell growth, migration, and invasion ability by MTT method and colony formation experiment. Luciferase reporter gene test assessed the relationship between SATB2-AS1 and TIMP2. LncRNA array analysis found significantly increased SATB2-AS1 expression in nasopharyngeal carcinoma tissues. Ectopic SATB2-AS1 overexpression in CNE1 cells promoted cell proliferation, migration, invasion and enhanced radiotherapy sensitivity. Bioinformatics and experiments confirmed that TIMP2 was a target of SATB2-AS1 and it participated in the upregulation of MMP-10 induced by SATB2-AS1. lncRNA SATB2-AS1 can promote the migration and invasion of nasopharyngeal carcinoma cells, indicating that it could be a potential marker for the treatment and prognosis.

scholarly journals Up-regulation of miR-34c-5p inhibits nasopharyngeal carcinoma cells by mediating NOTCH1

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Xin Xu ◽  
Haomin Yan ◽  
Le Zhang ◽  
Jing Liu ◽  
Yu Huang ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Biological Function ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Normal Cells ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Rescue Experiment ◽  
And Migration

Abstract Objective: To explore the correlation between miR-34c-5p and NOTCH1 in nasopharyngeal carcinoma (NPC). Materials and methods: qPCR was employed to quantify miR-34c-5p and NOTCH1 mRNA in NPC, and Western blot to detect NOTCH1. MiR-34c-5p mimics/inhibitor and NOTCH1 siRNA were constructed to analyze the role of miR-34c-5p/NOTCH1 on the biological function of NPC cells. Results: NPC cells showed lower miR-34c-5p expression and higher NOTCH1 expression than normal cells, and up-regulating miR-34c-5p or inhibiting NOTCH1 could strongly suppress the epithelial–mesenchymal transition (EMT), proliferation, invasion and migration of NPC cells, and induce apoptosis in them. Up-regulating miR-34c-5p could inhibit NOTCH1, and miR-34c-5p was negatively correlated with NOTCH1. Rescue experiment results revealed that NOTCH1 up-regulation could counteract the changes of cell process induced by increased miR-34c-5p. Conclusion: MiR-34c-5p inhibits the growth of NPC by down-regulating NOTCH1, so up-regulating miR-34c-5p or down-regulating NOTCH1 may become the potential direction of NPC treatment.

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