Properties of a non‐tumorigenic human cervical keratinocyte cell line

Stanley, Margaret; Browne, Helena; Appleby, Mark W.; Minson, A. C.

doi:10.1002/ijc.2910430422

Cited by 249 publications

(243 citation statements)

References 22 publications

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“…We investigated the miRNA expression profile in normal cervical tissue and cervical carcinoma cell lines SiHa and CaSki containing integrated HPV-16 DNA. We also used two clonal derivatives, 20861 and 201402, of the W12 cell line derived from a low-grade cervical intraepithelial neoplasia grade I (CIN I) lesion (Stanley et al, 1989), which contain integrated HPV-16 DNA (Alazawi et al, 2002). Significance analysis of microarray (SAM) analysis of the array data showed that 24 miRNAs, including miR-126, -143, -145 and miR-195 (four of the ten most highly expressed miRNAs in the normal cervix) were underexpressed in all the integrated HPV-16 cervical cell lines compared to the normal cervix (Table 1).…”

Section: Resultsmentioning

confidence: 99%

Human papillomavirus type 16 reduces the expression of microRNA-218 in cervical carcinoma cells

et al. 2007

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Human papillomaviruses (HPVs) are involved in the pathogenesis of cancer of the cervix (CaCx). MicroRNA (miRNA) expression analysis using Ambion (Austin, TX, USA) arrays showed that three miRNAs were overexpressed and 24 underexpressed in cervical cell lines containing integrated HPV-16 DNA compared to the normal cervix. Furthermore, nine miRNAs were overexpressed and one underexpressed in integrated HPV-16 cell lines compared to the HPV-negative CaCx cell line C-33A. Based on microarray and/or quantitative realtime PCR and northern blot analyses, microRNA-218 (miR-218) was specifically underexpressed in HPVpositive cell lines, cervical lesions and cancer tissues containing HPV-16 DNA compared to both C-33A and the normal cervix. Expression of the E6 oncogene of highrisk HPV-16, but not that of low-risk HPV-6, reduced miR-218 expression, and conversely, RNA interference of E6/E7 oncogenes in an HPV-16-positive cell line increased miR-218 expression. We also demonstrate that the epithelial cell-specific marker LAMB3 is a target of miR-218. We also show that LAMB3 expression is increased in the presence of the HPV-16 E6 oncogene and this effect is mediated through miR-218. These findings may contribute to a better understanding of the molecular mechanisms involved in cervical carcinogenesis.

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Section: Resultsmentioning

confidence: 99%

Human papillomavirus type 16 reduces the expression of microRNA-218 in cervical carcinoma cells

et al. 2007

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“…Establishment of HPV-16 immortalized cell lines W12, V1/G and AC89/E2 has been described previously (Stanley et al, 1989;Bouvard et al, 1996;Storey et al, 1992). Keratinocyte cell lines were grown in a 3 : 1 mixture of DMEM and Ham F12 medium, supplemented with 10% foetal calf serum, 10 ng/mL epidermal growth factor, 10 710 M cholera toxin and 0.4 mg/ mL hydrocortisone at 378C and 10% CO 2 .…”

Section: Cell Culture and Genotoxic Treatmentmentioning

confidence: 99%

Inhibition of E6 induced degradation of p53 is not sufficient for stabilization of p53 protein in cervical tumour derived cell lines

Mantovani

Banks

1999

Oncogene

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The E6 proteins derived from tumour associated papillomavirus types target the cellular tumour suppressor protein p53 for ubiquitin mediated degradation. In cell lines derived from cervical tumours the p53 protein is present in very low amounts, but it can be activated by appropriate DNA damaging agents, indicating that functional p53 is present within these lines. Recent studies have also shown that di erent polymorphic forms of the p53 protein are di erentially susceptible to E6 mediated degradation. Therefore we have been interested in analysing the e ects of di erent HPV E6 proteins upon p53 levels in a variety of cervical tumour derived cell lines. We show that inhibition of E6 mediated degradation of p53 frequently results in increased levels of p53 expression. However, there are notable exceptions to this where increased p53 levels are only obtained following DNA damage and proteasome inhibition. We also show in E6 expressing cells, that as well as p53 being targeted for degradation, the localization of p53 to the nucleus is also inhibited, consistent with previous observations which indicate that degradation of p53 is not essential for E6 mediated inhibition of p53 function. These results have important implications for any potential therapies which might aim to block E6 mediated degradation of p53.

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“…Little is known about the role of PTEN and LKB1 genes in (Dürst et al 1987a;Stanley et al 1989;Zheng et al 1994;Hietanen et al 1998). To establish an HPV-immortalized tonsillar epithelial cell line may provide a useful in vitro model to study HPV in tonsillar carcinogenesis.…”

Section: Introductionmentioning

confidence: 99%