Reexploring the Possible Roles of Some Genes Associated with Nasopharyngeal Carcinoma Using Microarray-based Detection

Fang, Wei; Liu, Teng Fei; Xie, Wei; Xu, Yang; Wang, Shuang; Ren, Cai ping; Deng, Xin; Liu, Qiu Zhen; Huang, Zhong; Li, Xin; Ding, Yan; Yao, Kai

doi:10.1111/j.1745-7270.2005.00074.x

Cited by 21 publications

(15 citation statements)

References 18 publications

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“…Recent studies showed that amplification of DNp63 gene and/or overexpression of DNp63 protein are frequent in human squamous carcinomas, including that of the head and neck (Thurfjell et al, 2004), bladder , esophagus (Taniere et al, 2001), lung (Massion et al, 2003), and nasopharynx (Crook et al, 2000;Fang et al, 2005). These observations suggest that DNp63 may have important implications in carcinogenesis.…”

mentioning

confidence: 95%

Overexpression of ΔNp63 in a human nasopharyngeal carcinoma cell line downregulates CKIs and enhances cell proliferation

Chiang

Chu

Chow

et al. 2008

Journal Cellular Physiology

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p63 belongs to a member of the tumor suppressor protein p53 family. Due to alternative promoter usage, two types of p63 proteins are produced. The DeltaNp63 isoform lacks the N-terminal transactivation domain and is thought to antagonize TAp63 and p53 in target gene regulation. DeltaNp63 has been found to be overexpressed in numerous human squamous cell carcinomas, including nasopharyngeal carcinoma (NPC). However, the role of DeltaNp63 overexpression in NPC pathogenesis has not been clear. In this study, we use a DeltaNp63 overexpressing human NPC cell line (NPC-076) to explore the possible roles of DeltaNp63 in cell proliferation and cell-cycle regulation. We found that the proliferation of NPC-076 cell is greatly suppressed when the overexpressed DeltaNp63 is silenced by specific DeltaNp63 siRNA. Further studies show that DeltaNp63 silencing results in the upregulation of CKIs, including p27(kip1) and p57(kip2) in both mRNA and protein levels. Cell-cycle analysis shows that DeltaNp63 silencing also results in an increased G1 phase cell and apoptotic cell population. Our findings indicate that DeltaNp63 plays important roles in the regulation of NPC-076 cell-cycle progression, and may play a role in the maintenance of NPC-076 tumor cell phenotype.

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mentioning

confidence: 95%

Overexpression of ΔNp63 in a human nasopharyngeal carcinoma cell line downregulates CKIs and enhances cell proliferation

Chiang

Chu

Chow

et al. 2008

Journal Cellular Physiology

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“…investigated a series of 16 low-grade gliomas and their subsequent progression to higher-grade malignancies using a one-megabase bacterial artificial chromosome (BAC)-based array comparative genomic hybridization technique, and reported that the CSE1L gene was associated with the progression of gliomas [40]. The results of another study using microarray-based detection showed that CSE1L was highly expressed in nasopharyngeal carcinomas [41]. Combined cytogenetic, array-based comparative genomic hybridization studies and expression analyses also showed that CSE1L was significantly overexpressed in advanced prostate cancer xenografts [42].…”

Section: Introductionmentioning

confidence: 99%

Cellular apoptosis susceptibility (CSE1L/CAS) protein in cancer metastasis and chemotherapeutic drug-induced apoptosis

Tai

Hsu

Shen

et al. 2010

J Exp Clin Cancer Res

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The cellular apoptosis susceptibility (CSE1L/CAS) protein is highly expressed in cancer, and its expression is positively correlated with high cancer stage, high cancer grade, and worse outcomes of patients. CSE1L (or CAS) regulates chemotherapeutic drug-induced cancer cell apoptosis and may play important roles in mediating the cytotoxicities of chemotherapeutic drugs against cancer cells in cancer chemotherapy. CSE1L was originally regarded as a proliferation-associated protein and was thought to regulate the proliferation of cancer cells in cancer progression. However, the results of experimental studies showed that enhanced CSE1L expression is unable to increase proliferation of cancer cells and CSE1L regulates invasion and metastasis but not proliferation of cancer cells. Recent studies revealed that CSE1L is a secretory protein, and there is a higher prevalence of secretory CSE1L in the sera of patients with metastatic cancer. Therefore, CSE1L may be a useful serological marker for screening, diagnosis and prognosis, assessment of therapeutic responses, and monitoring for recurrence of cancer. In this paper, we review the expression of CSE1L in cancer and discuss why CSE1L regulates the invasion and metastasis rather than the proliferation of cancer.

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“…Despite technical differences, our data included several of the key genes involved in apoptosis, cell cycle and oncogenesis (such as Bcl-2, p53, cyclin D2, claudin-1, centromere protein F, STAT1 and 2) that were similarly observed by Sriuranpong et al 5 , and in other NPC gene expression reports. [2][3][4][19][20][21] Pathways contributing to the development of nasopharyngeal carcinoma…”

Section: Immunohistochemistrymentioning

confidence: 99%

Multiple dysregulated pathways in nasopharyngeal carcinoma revealed by gene expression profiling

Shi¹,

Bastianutto²,

Li³

et al. 2006

Intl Journal of Cancer

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Gene expression profiling was conducted using primary human nasopharyngeal carcinoma (NPC) biopsy samples to improve the understanding of the molecular pathways defining NPC and to identify novel potential therapeutic targets. RNA samples were extracted from 36 patients suspected to have NPC and hybridized onto the Affymetrix U133A chip. NPC was diagnosed in 19 patients, 11 had lymphoid hyperplasia (LH), and 6 were “normal” biopsies. Clinical stages for these NPC patients ranged from I–IV, including one M1. All NPC patients (except the M1) were treated with curative intent, which included radiotherapy alone (4 patients), or combined with chemotherapy (14 patients). Unsupervised clustering demonstrated a distinct NPC expression pattern, compared to normal biopsies. Subsequent Significance Analysis of Microarrays (SAM) derived from 14 NPC and 6 normal samples discovered 1,089 differentially regulated genes. Pathway analyses revealed novel insights into the mechanisms leading to NPC, whereby upregulation of NFκB2 and survivin play central roles in increasing resistance to apoptosis, and changes in integrin and WNT/β‐catenin signaling leading to uncontrolled proliferation. The role of survivin in resisting apoptosis in NPC was confirmed by RNA interference. Our data provide novel insights into the development and progression of NPC, and suggest survivin as a novel therapeutic target for NPC. © 2006 Wiley‐Liss, Inc.

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Reexploring the Possible Roles of Some Genes Associated with Nasopharyngeal Carcinoma Using Microarray-based Detection

Cited by 21 publications

References 18 publications

Overexpression of ΔNp63 in a human nasopharyngeal carcinoma cell line downregulates CKIs and enhances cell proliferation

Overexpression of ΔNp63 in a human nasopharyngeal carcinoma cell line downregulates CKIs and enhances cell proliferation

Cellular apoptosis susceptibility (CSE1L/CAS) protein in cancer metastasis and chemotherapeutic drug-induced apoptosis

Multiple dysregulated pathways in nasopharyngeal carcinoma revealed by gene expression profiling

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