Telomerase activation cooperates with inactivation of p16 in early head and neck tumorigenesis

Soria, Jean‐Charles; Morat, Luc; Commo, Frédéric; Dabit, Dominique; Périé, Sophie; Sabatier, Laure; Fouret, Pierre

doi:10.1054/bjoc.2000.1647

Cited by 21 publications

(10 citation statements)

References 35 publications

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“…This leads to progression into the S phase (31). Studies have indicated that telomerase activity is correlated with high expression of cyclin D and low expression of p16INK4 (32)(33)(34). In the present study, inhibition of hTERT expression significantly altered the cell cycle profile of H1299 cells; the proportion of cells in G1 was increased (to 73.9%), while the percentage of cells in S and G2 phases was decreased.…”

Section: Discussionsupporting

confidence: 42%

Effect of plasmid-mediated RNA interference targeting telomerase reverse transcriptase on lung cancer cells

Deng

2011

Oncol Rep

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Abstract. In the present study, a plasmid-mediated siRNA interference vector targeting the hTERT gene was constructed and stably transfected into H1299 lung cancer cells. Using realtime quantitative fluorescent PCR technology, Western blotting and flow cytometry-based cell cycle profiling, the silencing effect of this vector and its inhibitory effect on proliferation in lung cancer cells were explored. Based upon the results of our previous study, a pair of siRNA sequences was selected, and a DNA template primer was designed and synthesized. After cloning of the template primer into the promoter of the pGenesil-1.1 expression vector, the constructed interference vector was validated using enzyme digestion and gene sequencing. The recombinant interference vector and empty vector were separately transfected into H1299 lung cancer cells with cationic liposomes, and stable monoclonally transfected cells were obtained after selection with G418. After stable transfection, hTERT mRNA and protein expression levels were detected using real-time RT-PCR technology and Western blotting. Using the MTT method and a colony formation assay, the growth and proliferation of the stably transfected lung cancer cells were determined. Changes in the cell cycle profile of the stably transfected lung cancer cells were detected using flow cytometry. An interference vector targeting the hTERT gene (pGenesil.1-hTERT) was successfully constructed. Enzyme digestion and gene sequencing confirmed that the sequence insertion met the criteria of the design. After transfection of H1299 cells with pGenesil

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Section: Discussionsupporting

confidence: 42%

Effect of plasmid-mediated RNA interference targeting telomerase reverse transcriptase on lung cancer cells

Deng

2011

Oncol Rep

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“…Second, the TRAP assay uses fresh or frozen tissue extracts and cannot identify which cells in tissue samples exhibit telomerase activity so that the precise contribution of infiltrating lymphocytes cannot be determined using this technique. [32][33][34] Therefore, in our present study, and for the first time, we have investigated the use of an RNA in situ hybridisation approach to elucidate the patterns of hTR RNA expression in OLP and normal buccal mucosal biopsies obtained from patients attending the Dublin Dental Hospital, Ireland.…”

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confidence: 99%

Telomerase activity detected in oral lichen planus by RNA in situ hybridisation: not a marker for malignant transformation

O’Flatharta

Leader

Kay

et al. 2002

Journal of Clinical Pathology

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Background: Oral lichen planus (OLP) is a chronic inflammatory condition. Clinically, it is characterised by the presence of a white lace-like lesion on the buccal mucosa, tongue, and gingivae, with erosions and ulceration. The World Health Organisation considers OLP to be a premalignant condition. Aims: To investigate expression of the telomerase RNA component (hTR) in OLP compared with normal control buccal mucosa and to assess the possibility of using hTR expression as a marker for malignant transformation in OLP. Methods: hTR expression was analysed in 40 cases of OLP and 18 normal control buccal mucosa samples using an RNA in situ hybridisation approach. Results: Strong hTR RNA expression was seen in the basal, suprabasal, and to a lesser extent in the upper epithelial layers in 36 of the 40 OLP lesions examined. Infiltrating subepithelial lymphocytes in OLP were also shown to express hTR RNA. Weak hTR RNA expression was seen in seven of the 18 normal control buccal mucosa specimens, with expression confined exclusively to the basal layer of the epithelium and absent in the suprabasal and upper layers. Conclusion: The telomerase RNA component hTR is found to be highly expressed in the epithelium of non-dysplastic OLP lesions. It is possible that this high expression is related to the increased cellular proliferation seen in OLP lesions rather than being an indicator of susceptibility to malignancy. Thus, hTR RNA expression may not be a suitable marker for predicting malignant transformation in OLP.

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“…Similarly, Chen observed an increasing trend of p16 staining score with increasing grades of dysplasia (Chen et al , 1999). Conversely, several investigators have found a significant correlation between decreased p16 protein expression and histologic grade of dysplasia (Soria et al , 2001; Shintani et al , 2002; Bradley et al , 2006). While not the focus of this review, it should be noted that overexpression of p16 in SCC is now used as a surrogate for identifying HPV‐associated SCC vs SCC associated with tobacco and alcohol consumption.…”

Section: Rb Family: Rb P16mentioning

confidence: 94%

Genetics/epigenetics of oral premalignancy: current status and future research*

et al. 2011

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Oral Diseases (2011) 17 (Suppl. 1), 7–22 Squamous cell carcinoma (SCC) of the oral and oropharyngeal region is the sixth most common malignancy in the world today. Despite numerous advances in treatment, long‐term survival from this disease remains poor. Early detection can decrease both morbidity and mortality associated with this neoplasm. However, screening for potentially malignant disease is typically confounded by difficulty in discriminating between reactive/inflammatory lesions vs those lesions that are premalignant in nature. Furthermore, the histologic diagnosis of dysplasia can be subjective and is thus prone to a considerable range of interpretation. Similarly, no definitive, validated criteria exist for predicting which dysplastic lesions are most likely to progress to cancer over time. Given this state of science, the presence of dysplasia can only be used to indicate that an oral lesion may have an increased risk of malignant transformation. Molecular biomarkers capable of identifying the subset of lesions likely to progress to cancer are required to eliminate this clinical diagnostic dilemma. The purpose of this review is to assess the current state of knowledge regarding genetic/epigenetic alterations observed in oral mucosal premalignancy. In addition, recommendations for future research studies directed at defining the predictive capacity of specific biomarkers in this modeling are presented.

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Telomerase activation cooperates with inactivation of p16 in early head and neck tumorigenesis

Cited by 21 publications

References 35 publications

Effect of plasmid-mediated RNA interference targeting telomerase reverse transcriptase on lung cancer cells

Effect of plasmid-mediated RNA interference targeting telomerase reverse transcriptase on lung cancer cells

Telomerase activity detected in oral lichen planus by RNA in situ hybridisation: not a marker for malignant transformation

Genetics/epigenetics of oral premalignancy: current status and future research*

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