scholarly journals Study of miR-10b regulatory mechanism for epithelial-mesenchymal transition, invasion and migration in nasopharyngeal carcinoma cells

2017 ◽  
Author(s):  
Weiyi Wang
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Regulatory Mechanism ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration

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.

scholarly journals Benzotriazole Enhances Cell Invasive Potency in Endometrial Carcinoma Through CTBP1-Mediated Epithelial-Mesenchymal Transition

2017 ◽  
Vol 44 (6) ◽  
pp. 2357-2367 ◽  
Author(s):  
Yiquan Wang ◽  
Chencheng Dai ◽  
Cheng Zhou ◽  
Wenqu Li ◽  
Yujia Qian ◽  
...  
Keyword(s):  
Endometrial Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Expression Patterns ◽  
Underlying Mechanism ◽  
Carcinoma Cells ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Female Reproductive Health ◽  
Gene Microarray Analysis ◽  
And Migration

Background/Aims: Benzotriazole (BTR) and its derivatives, such as intermediates and UV stabilizers, are important man-made organic chemicals found in everyday life that have been recently identified as environmental toxins and a threat to female reproductive health. Previous studies have shown that BTR could act as a carcinogen by mimicking estrogen. Environmental estrogen mimics could promote the initiation and development of female cancers, such as endometrial carcinoma, a type of estrogenic-sensitive malignancy. However, there is little information on the relationship between BTR and endometrial carcinoma. In this study, we aimed to demonstrate the biological function of BTR in endometrial carcinoma and explored the underlying mechanism. Methods: The CCK-8 assay was performed to detect cell viability; transwell-filter assay was used to assess cell invasion; gene microarray analysis was employed to determine gene expression patterns in response to BTR treatment; western blotting and quantitative reverse transcription polymerase chain reaction (qRT-PCR) were carried out to detect the expression levels of BTR-related genes. Results: Our data showed that BTR could induce the invasion and migration of endometrial carcinoma cells (Ishikawa and HEC-1-B). In addition, BTR increased the expression level of CTBP1, which could enhance the epithelial-mesenchymal transition (EMT) in cancer cells. Moreover, CTBP1 silencing reversed the effect of BTR on EMT progression in endometrial carcinoma cells. Conclusion: This study indicates that BTR could act as a carcinogen to promote the development of endometrial carcinoma mainly through CTBP1-mediated EMT, which deserves more attention.

scholarly journals A long non-coding RNA lncRNA-PE promotes invasion and epithelial–mesenchymal transition in hepatocellular carcinoma through the miR-200a/b-ZEB1 pathway

Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831770575 ◽  
Author(s):  
Yuan Shen ◽  
Shanshan Liu ◽  
Hanyu Yuan ◽  
Xiaomin Ying ◽  
Hanjiang Fu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Human Hepatocellular Carcinoma ◽  
Tissue Samples ◽  
Hepatocellular Carcinoma Cells ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Non Coding Rnas ◽  
And Migration

Long non-coding RNAs have been revealed to play important roles in the progression of hepatocellular carcinoma. However, the detailed mechanisms underlying their activities are not fully understood. Using microarray technology, a number of long non-coding RNAs were previously identified to be aberrantly expressed in hepatocellular carcinoma. In this study, one of these long non-coding RNAs, designated lncRNA-PE (lncRNA promotes epithelial–mesenchymal transition), was further explored to study its expression profile and function. A cohort of human hepatocellular carcinoma tissue samples combined with benign controls and established human hepatocellular carcinoma cell lines were examined for the expression of lncRNA-PE. The biological functions of lncRNA-PE were examined by wound-healing and Transwell assays, which revealed that lncRNA-PE promotes cell invasion and migration. By detecting the level of epithelial–mesenchymal transition markers, lncRNA-PE was revealed to promote epithelial–mesenchymal transition in hepatocellular carcinoma cells. Further study suggested that lncRNA-PE downregulated miR-200a/b by repressing the primary transcript expression, enhanced ZEB1 expression, and promoted epithelial–mesenchymal transition of hepatocellular carcinoma cells. All these data imply that lncRNA-PE might play an important role in hepatocellular carcinoma development via the miR-200a/b-ZEB1 pathway.

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.

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