MicroRNAs: novel factors in clinical diagnosis and prognosis for nasopharyngeal carcinoma
MicroRNAs: novel factors in clinical diagnosis and prognosis for nasopharyngeal carcinoma
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MicroRNA:鼻咽癌临床诊断和预后的新因素
DOI:
10.1038/aps.2012.98
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发表时间:
2012-07
影响因子:
8.2
通讯作者:
Li, Yao
中科院分区:
文献类型:
--
作者:
Yang, Shu;Li, Yao
Nasopharyngeal carcinoma (NPC) is a non-lymphomatous, squamous cell malignancy arising from the epithelial cells lining of the nasopharynx. Histologically, NPC has been classified into 3 types: keratinizing squamous cell carcinoma (WHO type I), differentiated non-keratinizing squamous cell carcinoma (WHO type II) and undifferentiated carcinomas (WHO type III). Compared to other malignant tumours of the upper aero digestive tract, NPC is a special type of head and neck cancer in terms of epidemiology, pathology and clinical presentation. The etiology of NPC involves multiple factors, including genetic susceptibility, exposure to chemical carcinogens and Epstein-Barr virus (EBV) infection [1]. In some regions, notably the southern parts of China, and parts of Southeast Asia, this cancer occurs in an endemic form with an incidence 10-to 30-fold higher than in the other regions and, histologically, usually belongs to WHO type II and III. In the west, however, NPC occurs sporadically and usually belongs to WHO type I. There is also increased incidence in northern Africa and the Inuit of Alaska [2, 3]. MicroRNAs (miRNAs) are a class of small non-coding RNA molecules, 19–25 nucleotides in length, that negatively regulate gene expression through binding the 3’-untranslated region (3’-UTR) of targeted transcripts, resulting in mRNA cleavage or translation repression [4]. About 30% of human genes are regulated by miRNAs. MicroRNAs are frequently deregulated in many types of cancers, and play critical roles in tumorigenesis, which regulate the expression of oncogenes or tumour suppressor genes. In a recent issue of Lancet Oncol, Liu et al [5] reported that 41 miRNAs were differentially expressed between nasopharyngeal carcinoma and noncancer nasopharyngitis tissues (fold change≥ 2.5, false discovery rate 0). Previous reports showed that miRNAs were aberrantly expressed in nasopharyngeal carcinoma compared with normal epithelial tissue, and promoted an aggressive tumour phenotype by changing the expression of their mRNA targets [6–8]. For instance, Sengupta et al [6] investigated the expressions of 207 miRNAs in 31 NPCs and 10 normal tissues with miRNA microarrays, and demonstrated the involvement of miR-29c in NPC metastasis by regulating mRNAs encoding extracellular matrix proteins. Chen et al [7] studied the expression of 270 human miRNAs in 13 NPC samples in comparison with 9 adjacent normal tissues using a stemloop real-time PCR assay, and found the expressions of 35 miRNAs were significantly altered in NPC, thus inferred that some cancer-related pathways enriched with targets of down-regulated miRNAs. We also demonstrated with microarray that 34 miRNAs were differentially expressed between 8 NPC and 4 normal tissues [8]. Furthermore, we identified 2 novel pathways, targeted by the altered miRNAs, were strongly associated with NPC development, and a c-Myc centred miRNA regulatory network was inferred in NPC. These reports indicate that some important miRNAs can be used as markers for differential diagnosis of NPC from non-cancer nasopharyngitis patients. Interestingly, in all the 4 studies, miR-34c has been found underexpression in NPC specimens, suggesting that that this miRNA plays a crucial role in NPC development and progression. However, the functions of miR-34c were still unclear in NPC. Additionally, 3 out of the 4 reports showed that 3 miRNAs (miR-34b, miR-29c and miR-100) in NPC were downregulated. Here, we pay attention to the miR-29 family because miR-29a and miR-29b were also under-expressed in NPC as shown in 2 of the 4 reports. We consider that the miR-29 …
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DOI:
10.1016/b978-0-12-814936-2.00002-x
发表时间:
2019
期刊:
Nasopharyngeal Carcinoma
影响因子:
--
作者:
M. Lung;Wei Dai;J. Ko
通讯作者:
M. Lung;Wei Dai;J. Ko
影响因子:
2.1
作者:
Carle, Laura N.;Ko, Charles C.;Castle, James T.
通讯作者:
Castle, James T.
影响因子:
3.3
作者:
Chong, V. F. H.;Ong, C. K.
通讯作者:
Ong, C. K.
影响因子:
51.1
作者:
Liu, Na;Chen, Nian-Yong;Ma, Jun
通讯作者:
Ma, Jun
影响因子:
1.9
作者:
Kamran, Sophia C.;Riaz, Nadeem;Lee, Nancy
通讯作者:
Lee, Nancy