Genome‐wide profiling of oral squamous cell carcinoma

Chen, Yann Jang; Lin, Shu Chun; Kao, Tsai; Chang, Che Shoa; Hong, Pei; Shieh, Tzong‐Ming; Chang, Kuo Wei

doi:10.1002/path.1640

Cited by 142 publications

(113 citation statements)

References 13 publications

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“…Recent studies showed that Bmi-1 is a direct transcriptional target of c-Myc in human fibroblasts (Guney et al, 2006) and of E2F-1 in neuroblastomas (Nowak et al, 2006). c-Myc was found to be frequently amplified in OSCCs by comparative genomic hybridisation (Chen et al, 2004). Thus, c-Myc-dependent Bmi-1 promoter activation may account for the enhanced gene expression during dysplastic cell transformation in oral carcinogenesis, although the extent to which c-Myc regulates the Bmi-1 promoter activity in oral carcinogenesis needs further investigation.…”

Section: Discussionmentioning

confidence: 99%

Elevated Bmi-1 expression is associated with dysplastic cell transformation during oral carcinogenesis and is required for cancer cell replication and survival

Mk¹,

Kim²,

Sj³

et al. 2006

Br J Cancer

142

125

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Bmi-1 is a polycomb group protein that was identified as c-myc cooperating oncogene in murine lymphomagenesis. The current study was undertaken to determine the role of Bmi-1 in human oral carcinogenesis. Bmi-1 protein and RNA expression levels were markedly enhanced in the cells of oral squamous cell carcinomas (OSCC) compared with that of normal human oral keratinocytes (NHOK). Enhanced-Bmi-1 expression was also detected in situ in the archived oral mucosal tissues with cancerous and precancerous histopathology, including that of mild epithelial dysplasia. Thus, Bmi-1 expression occurs at a very early stage in oral carcinogenesis. To determine the biological role of Bmi-1 in cell proliferation, endogenous Bmi-1 was knocked down in actively proliferating SCC4 cells and NHOK by RNA interference. After Bmi-1 knockdown, cell replication was severely retarded. However, the expression of p16 INK4A , a known cellular target of Bmi-1, was not changed in cells with or without Bmi-1 knockdown. Furthermore, Bmi-1 knockdown in HOK-16B-BaP-T cells, in which the p16 INK4A /pRb pathway was abrogated, led to immediate arrest of replication and loss of viable cells. Thus, our data suggest that Bmi-1 may act through p16 INK4A -independent pathways to regulate cellular proliferation during oral cancer progression.

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Section: Discussionmentioning

confidence: 99%

Elevated Bmi-1 expression is associated with dysplastic cell transformation during oral carcinogenesis and is required for cancer cell replication and survival

Mk¹,

Kim²,

Sj³

et al. 2006

Br J Cancer

142

125

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“…Amplification of this region in HNSCC has been associated with decreased survival (Akervall et al, 1995;Meredith et al, 1995), increased distant metastasis (Namazie et al, 2002) and lymph node metastasis (Chen et al, 2004;Hermsen et al, 2005;Xia et al, 2007). It is believed that amplification increases gene dosage and expression of genes within the amplified region (amplicon) (Albertson, 2006).…”

mentioning

confidence: 99%

Cortactin expression predicts poor survival in laryngeal carcinoma

et al. 2008

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Amplification of the 11q13 region is one of the most frequent aberrations in squamous cell carcinomas of the head and neck region (HNSCC). Amplification of 11q13 has been shown to correlate with the presence of lymph node metastases and decreased survival. The 11q13.3 amplicon carries numerous genes including cyclin D1 and cortactin. Recently, we reported that FADD becomes overexpressed upon amplification and that FADD protein expression predicts for lymph node positivity and disease-specific mortality. However, the gene within the 11q13.3 amplicon responsible for this correlation is yet to be identified. In this paper, we compared, using immunohistochemical analysis for cyclin D1, FADD and cortactin in a series of 106 laryngeal carcinomas which gene correlates best with lymph node metastases and increased disease-specific mortality. Univariate Cox regression analysis revealed that high expression of cyclin D1 (P ¼ 0.016), FADD (P ¼ 0.003) and cortactin (P ¼ 0.0006) predict for increased risk to disease-specific mortality. Multivariate Cox analysis revealed that only high cortactin expression correlates with disease-specific mortality independent of cyclin D1 and/or FADD. Of genes located in the 11q13 amplicon, cortactin expression is the best predictor for shorter diseasespecific survival in late stage laryngeal carcinomas. Current methods to predict the outcome of head and neck squamous cell carcinoma (HNSCC) patients mainly involve clinicopathological parameters such as tumour size, differentiation grade and presence of lymph node metastasis. Patients with laryngeal squamous cell carcinomas (LSCC) have not shown an increase in 5-year survival rates over the last 30 years (Almadori et al, 2005). Therefore, other parameters such as molecular markers that are able to more accurately predict the outcome of disease, are needed.A frequent molecular event in HNSCC is amplification of the 11q13 region (36%) (Schuuring, 1995;Freier et al, 2006). Amplification of this region in HNSCC has been associated with decreased survival (Akervall et al, 1995;Meredith et al, 1995), increased distant metastasis (Namazie et al, 2002) and lymph node metastasis (Chen et al, 2004;Hermsen et al, 2005;Xia et al, 2007). It is believed that amplification increases gene dosage and expression of genes within the amplified region (amplicon) (Albertson, 2006). Recently, we reported that the commonly amplified region is located at 11q13.3 and contains at least six genes (cyclin D1, TAOS1, FGF19, FADD, PPFIA1 and cortactin) that are overexpressed when amplified (Gibcus et al, 2007b). We concluded that the selection for tumour cells with the 11q13.3 amplicon during tumorigenesis could be based on the increased doses of one or more of these genes. We proposed FADD as a possible candidate for this selection, since FADD showed the best correlation between DNA amplification and increased expression (Gibcus et al, 2007b). Furthermore, FADD protein expression correlated with disease specific mortality (DSM) in a series of late stage laryngeal carcinom...

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“…1,2 Areca chewing is epidemiologically linked to the high incidence of oral squamous cell carcinoma (OSCC) and other oral lesions in this population. 3,4 Areca nuts contain polyphenols, arecoline, arecaidine and other ingredients.…”

mentioning

confidence: 99%

Areca (betel) nut extract activates mitogen‐activated protein kinasesand NF‐κB in oral keratinocytes

Lin

Lee

et al. 2005

Intl Journal of Cancer

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Areca (betel) was recently proved a carcinogenic substance by the International Agency for Research on Cancer. However, the signaling impact of areca in oral keratinocyte is still obscure. Mitogen‐activated protein kinase superfamilies, including extracellular signal‐regulated kinase (ERK), c‐Jun N‐terminal kinases (JNK) and p38, together with transcription factor NF‐κB, are important signaling elements. We examined the activation of these signaling pathways in OECM‐1 and SAS oral keratinocytes, treated with ripe areca nut extract (ANE). In both cells, a rapid increase in JNK1 activity at 0.5 hr was noted following treatment of ANE. ERK was profoundly activated during 0.5–2 hr in OECM‐1 cells. Contrasting p38 activity was noted in these 2 cells. In both cells, ANE also activated NF‐κB pathway in a biphasic manner, particularly for SAS cells. NF‐κB was activated by ∼ 2‐ to 4‐fold at 0.5–1 hr and a plateau or slight decrease of activity existed between 1 and 6 hr. Later, another higher episode of NF‐κB activity was raised. This was accompanied with the rapid degradation in cytosolic IκBα as well as an increase of nuclear NF‐κB in both cells. ANE treatment did not activate epidermal growth factor receptor signaling system, but blockage of NF‐κB activation rendered the suppression of ANE‐modulated COX‐2 upregulation in OECM‐1. This study identified that ANE affected interactive signaling systems in oral keratonocytes that could be the pathogenetic basis for areca. © 2005 Wiley‐Liss, Inc.

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Genome‐wide profiling of oral squamous cell carcinoma

Cited by 142 publications

References 13 publications

Elevated Bmi-1 expression is associated with dysplastic cell transformation during oral carcinogenesis and is required for cancer cell replication and survival

Elevated Bmi-1 expression is associated with dysplastic cell transformation during oral carcinogenesis and is required for cancer cell replication and survival

Cortactin expression predicts poor survival in laryngeal carcinoma

Areca (betel) nut extract activates mitogen‐activated protein kinasesand NF‐κB in oral keratinocytes

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