scholarly journals Down-regulation of the microRNA-99 family members in head and neck squamous cell carcinoma

Oral Oncology ◽  
2012 ◽  
Vol 48 (8) ◽  
pp. 686-691 ◽  
Author(s):  
Zujian Chen ◽  
Yi Jin ◽  
Dongsheng Yu ◽  
Anxun Wang ◽  
Ishrat Mahjabeen ◽  
...  
2018 ◽  
Vol 97 (6) ◽  
pp. 645-653 ◽  
Author(s):  
T. Fukusumi ◽  
J.A. Califano

Comprehensive genomic analyses have been performed for head and neck squamous cell carcinoma (HNSCC), revealing a significant rate of NOTCH1 mutations and identifying NOTCH1 as the second most frequently mutated gene after TP53. Most NOTCH1 mutations are considered inactivating, indicating that NOTCH1 is a tumor suppressor gene. On the other hand, cohorts from Asian populations with HNSCC have shown activating NOTCH1 mutations. HNSCC with NOTCH1 mutations have a worse prognosis than the NOTCH1 wild-type tumors. Additional data on other NOTCH family members have shown that NOTCH promotes HNSCC progression. NOTCH family members, including NOTCH pathway genes, are upregulated in HNSCC compared with normal tissues, and inhibition of the NOTCH pathway decreases cell proliferation and invasion. NOTCH activity in HNSCC is therefore contextual, and NOTCH in HNSCC is considered to have a bimodal role as a tumor suppressor and an oncogene. In this review, recent understandings of NOTCH pathway genes, including NOTCH genes, in HNSCC are described. In addition, the implications of NOTCH pathway alteration for HNSCC-specific NOTCH-targeted cancer therapy are explored.


Head & Neck ◽  
2015 ◽  
Vol 38 (S1) ◽  
pp. E934-E940 ◽  
Author(s):  
Sang Hyeok Woo ◽  
Liang P. Yang ◽  
Hui-Ching Chuang ◽  
Alison Fitzgerald ◽  
Ho-Young Lee ◽  
...  

2005 ◽  
Vol 11 (8) ◽  
pp. 2937-2946 ◽  
Author(s):  
Akihiro Katayama ◽  
Takeshi Ogino ◽  
Nobuyuki Bandoh ◽  
Satoshi Nonaka ◽  
Yasuaki Harabuchi

2021 ◽  
Vol 11 ◽  
Author(s):  
Tingting Zhang ◽  
Xueqin Zhu ◽  
Qiang Sun ◽  
Xing Qin ◽  
Zhen Zhang ◽  
...  

Constituents of tobacco that can cause DNA adduct formation and oxidative stress are implicated in the development of head and neck squamous cell carcinoma (HNSCC). However, there are few studies on the mechanism(s) that underlie tobacco-associated HNSCC. Here, we used a model in which tumors were induced in rats using 4-nitroquinoline 1-oxide (4NQO), which mimicked tobacco-related HNSCC, and analyzed the expression profiles of microRNAs and mRNAs. Our results indicated that 57 miRNAs and 474 mRNA/EST transcripts exhibited differential expression profiles between tumor and normal tongue tissues. In tumor tissue, the expression levels of rno-miR-30 family members (rno-miR-30a, rno-miR-30a-3p, rno-miR-30b-5p, rno-miR-30c, rno-miR-30d, rno-miR-30e and rno-miR-30e-3p) were only 8% to 37% of those in the control group. The GO terms enrichment analysis of the differentially expressed miRNAs indicated that oxidation reduction was the most enriched process. Low expression of miR-30 family members in human HNSCC cell lines and tissues was validated by qPCR. The results revealed that the expression of miR-30b-5p and miR-30e-5p was significantly decreased in the TCGA HNSCC dataset and validation datasets, and this decrease in expression further distinguishes HNSCC associated with tobacco use from other subtypes of HNSCC. CCK8, colony formation, transwell migration and HNSCC xenograft tumor assays indicated that miR-30b-5p or miR-30e-5p inhibited proliferation, migration and invasion in vitro, and miR-30b-5p suppressed tumor growth in vivo. Moreover, we uncovered that KRAS might be the potential target gene of miR-30e-5p or miR-30b-5p. Thus, our data clearly showed that decreased expression of miR-30e-5p or miR-30b-5p may play a crucial role in cancer development, especially that of tobacco-induced HNSCC, and may be a novel candidate biomarker and target for this HNSCC subtype.


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