Knockdown of LINC01116 inhibits cell migration and invasion in head and neck squamous cell carcinoma through epithelial‐mesenchymal transition pathway

2019 ◽  
Vol 121 (1) ◽  
pp. 867-875 ◽  
Author(s):  
Jing Wu ◽  
Zhizhao Chen ◽  
Li Zhang ◽  
Jun Cao ◽  
Xiaoyu Li ◽  
...  
Cancers ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 395 ◽  
Author(s):  
Chris Yang ◽  
Wafik Sedhom ◽  
John Song ◽  
Shi-Long Lu

Head and neck squamous cell carcinoma (HNSCC) affects 650,000 people worldwide and has a dismal 50% 5-year survival rate. Recurrence and metastasis are believed the two most important factors causing this high mortality. Understanding the biological process and the underlying mechanisms of recurrence and metastasis is critical to develop novel and effective treatment, which is expected to improve patients’ survival of HNSCC. MicroRNAs are small, non-coding nucleotides that regulate gene expression at the transcriptional and post-transcriptional level. Oncogenic and tumor-suppressive microRNAs have shown to regulate nearly every step of recurrence and metastasis, ranging from migration and invasion, epithelial-mesenchymal transition (EMT), anoikis, to gain of cancer stem cell property. This review encompasses an overview of microRNAs involved in these processes. The recent advances of utilizing microRNA as biomarkers and targets for treatment, particularly on controlling recurrence and metastasis are also reviewed.


2011 ◽  
Vol 440 (1) ◽  
pp. 23-31 ◽  
Author(s):  
Xiqiang Liu ◽  
Cheng Wang ◽  
Zujian Chen ◽  
Yi Jin ◽  
Yun Wang ◽  
...  

Down-regulation of miR-138 (microRNA-138) has been frequently observed in various cancers, including HNSCC (head and neck squamous cell carcinoma). Our previous studies suggest that down-regulation of miR-138 is associated with mesenchymal-like cell morphology and enhanced cell migration and invasion. In the present study, we demonstrated that these miR-138-induced changes were accompanied by marked reduction in E-cad (E-cadherin) expression and enhanced Vim (vimentin) expression, characteristics of EMT (epithelial–mesenchymal transition). On the basis of a combined experimental and bioinformatics analysis, we identified a number of miR-138 target genes that are associated with EMT, including VIM, ZEB2 (zinc finger E-box-binding homeobox 2) and EZH2 (enhancer of zeste homologue 2). Direct targeting of miR-138 to specific sequences located in the mRNAs of the VIM, ZEB2 and EZH2 genes was confirmed using luciferase reporter gene assays. Our functional analyses (knock-in and knock-down) demonstrated that miR-138 regulates the EMT via three distinct pathways: (i) direct targeting of VIM mRNA and controlling the expression of VIM at a post-transcriptional level, (ii) targeting the transcriptional repressors (ZEB2) which in turn regulating the transcription activity of the E-cad gene, and (iii) targeting the epigenetic regulator EZH2 which in turn modulates its gene silencing effects on the downstream genes including E-cad. These results, together with our previously observed miR-138 effects on cell migration and invasion through targeting RhoC (Rho-related GTP-binding protein C) and ROCK2 (Rho-associated, coiled-coil-containing protein kinase 2) concurrently, suggest that miR-138 is a multi-functional molecular regulator and plays major roles in EMT and in HNSCC progression.


2020 ◽  
Vol 16 (28) ◽  
pp. 2209-2218
Author(s):  
Li Zhang ◽  
Hao Bo ◽  
Tingwei Chen ◽  
Qiaohua Li ◽  
Ye Huan ◽  
...  

Aim: To investigate the role of long noncoding RNA FOXD2-AS1 in head and neck squamous cell carcinoma (HNSCC). Materials & methods: The expression and clinical significance of FOXD2-AS1 were analyzed using data from public databases. Transwell assays were used to examine the function of FOXD2-AS1 in HNSCC. The molecular mechanism of FOXD2-AS1 was probed by western blotting. Results: The expression of FOXD2-AS1 was upregulated in HNSCC; it was positively related with the pathological stage as well as with poor prognosis in HNSCC patients. FOXD2-AS1 silencing inhibited HNSCC cell migration and invasion, also influenced the expression of epithelial–mesenchymal transition-related molecules. Conclusion: FOXD2-AS1 was a prognostic marker in patients with HNSCC and may be a favorable novel treatment target for HNSCC.


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