scholarly journals Screening and identification of potential target genes in head and neck cancer using bioinformatics analysis

2019 ◽  
Author(s):  
Fuhai Chen ◽  
Anyuan Zheng ◽  
Fen Li ◽  
Silu Wen ◽  
Shiming Chen ◽  
...  
2018 ◽  
Vol 74 ◽  
pp. 291-295 ◽  
Author(s):  
Canhua Xiao ◽  
Jonathan J. Beitler ◽  
Kristin A. Higgins ◽  
Evanthia C. Wommack ◽  
Nabil F. Saba ◽  
...  

Cancers ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 856
Author(s):  
Junichiro Chikuda ◽  
Kurataka Otsuka ◽  
Iwao Shimomura ◽  
Kagenori Ito ◽  
Hiroaki Miyazaki ◽  
...  

Cisplatin (cis-diamminedichloroplatinum II [CDDP] ) is a well-known chemotherapeutic drug that has been used for the treatment of various types of human cancers, including head and neck cancer. Cisplatin exerts anticancer effects by causing DNA damage, replication defects, transcriptional inhibition, cell cycle arrest, and the induction of apoptosis. However, drug resistance is one of the most serious problems with cancer chemotherapy, and it causes expected therapeutic effects to not always be achieved. Here, we analyzed global microRNA (miRNA) expression in CD44 standard form (CD44s)-expressing SAS cells, and we identified miR-629-3p as being responsible for acquiring anticancer drug resistance in head and neck cancer. The introduction of miR-629-3p expression inhibited apoptotic cell death under cisplatin treatment conditions, and it promoted cell migration. Among the computationally predicted target genes of miR-629-3p, we found that a number of gene expressions were suppressed by the transfection with miR-629-3p. Using a xenografting model, we showed that miR-629-3p conferred cisplatin resistance to SAS cells. Clinically, increased miR-629-3p expression tended to be associated with decreased survival in head and neck cancer patients. In conclusion, our data suggest that the increased expression of miR-629-3p provides a mechanism of cisplatin resistance in head and neck cancer and may serve as a therapeutic target to reverse chemotherapy resistance.


2019 ◽  
Author(s):  
Emilie A. Warren ◽  
Hsuan-Chen Liu ◽  
Caroline E. Porter ◽  
Kershena S. Liao ◽  
Meenakshi Hegde ◽  
...  

2019 ◽  
Author(s):  
Emilie A. Warren ◽  
Hsuan-Chen Liu ◽  
Caroline E. Porter ◽  
Kershena S. Liao ◽  
Meenakshi Hegde ◽  
...  

BMC Genetics ◽  
2016 ◽  
Vol 17 (1) ◽  
Author(s):  
Cielito C. Reyes-Gibby ◽  
Jian Wang ◽  
Mary Rose T. Silvas ◽  
Robert Yu ◽  
Sai-Ching J. Yeung ◽  
...  

2013 ◽  
Vol 19 (9) ◽  
pp. 2528-2540 ◽  
Author(s):  
Jong-Lyel Roh ◽  
Xin Victoria Wang ◽  
Judith Manola ◽  
David Sidransky ◽  
Arlene A. Forastiere ◽  
...  

2018 ◽  
Vol 97 (6) ◽  
pp. 665-673 ◽  
Author(s):  
K.A. Alamoud ◽  
M.A. Kukuruzinska

Head and neck cancer presents primarily as head and neck squamous cell carcinoma (HNSCC), a debilitating malignancy fraught with high morbidity, poor survival rates, and limited treatment options. Mounting evidence indicates that the Wnt/β-catenin signaling pathway plays important roles in the pathobiology of HNSCC. Wnt/β-catenin signaling affects multiple cellular processes that endow cancer cells with the ability to maintain and expand immature stem-like phenotypes, proliferate, extend survival, and acquire aggressive characteristics by adopting mesenchymal traits. A central component of canonical Wnt signaling is β-catenin, which balances its role as a structural component of E-cadherin junctions with its function as a transcriptional coactivator of numerous target genes. Recent genomic characterization of head and neck cancer revealed that while β-catenin is not frequently mutated in HNSCC, its activity is unchecked by more common mutations in genes encoding upstream regulators of β-catenin, NOTCH1, FAT1, and AJUBA. Wnt/β-catenin signaling affects a wide range epigenetic and transcriptional activities, mediated by the interaction of β-catenin with different transcription factors and transcriptional coactivators and corepressors. Furthermore, Wnt/β-catenin functions in a network with many signaling and metabolic pathways that modulate its activity. In addition to its effects on tumor epithelia, β-catenin activity regulates the tumor microenvironment by regulating extracellular matrix remodeling, fibrotic processes, and immune response. These multifunctional oncogenic effects of β-catenin make it an attractive bona fide target for HNSCC therapy.


2016 ◽  
Vol 18 (2) ◽  
pp. 232-253 ◽  
Author(s):  
Javadi Monisha ◽  
Nand Kishor Roy ◽  
Devivasha Bordoloi ◽  
Amit Kumar ◽  
Ramesh Golla ◽  
...  

2013 ◽  
Author(s):  
Yi-Zih Kuo ◽  
Yun-Chu Huang ◽  
Yuh-Ling Chen ◽  
Hung-I Lo ◽  
Sen-Tien Tsai ◽  
...  

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