Different human cervical carcinoma cell lines show similar transcription patterns of human papillomavirus type 18 early genes.

Schneider-Gädicke, Ansbert; Schwarz, Elisabeth

doi:10.1002/j.1460-2075.1986.tb04496.x

Cited by 416 publications

(333 citation statements)

References 37 publications

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“…For the detection of HPV RNA products, we used a cDNA termed 1 3 containing the E6* and E7 coding information on a 683 bp EcoRI-HindIII fragment derived from cDNA H4 (Schneider-Gädicke & Schwarz 1986, Roggenbuck et al 1990) in vector pGEM-3. This clone was kindly provided by Elisabeth Schwarz (DKFZ, Heidelberg, Germany).…”

Section: Probesmentioning

confidence: 99%

Evidence for a nuclear compartment of transcription and splicing located at chromosome domain boundaries

et al. 1993

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The nuclear topography of splicing snRNPs, mRNA transcripts and chromosome domains in various mammalian cell types are described. The visualization of splicing snRNPs, defined by the Sm antigen, and coiled bodies, revealed distinctly different distribution patterns in these cell types. Heat shock experiments confirmed that the distribution patterns also depend on physiological parameters. Using a combination of fluorescence in situ hybridization and immunodetection protocols, individual chromosome domains were visualized simultaneously with the Sm antigen or the transcript of an integrated human papilloma virus genome. Three-dimensional analysis of fluorescence-stained target regions was performed by confocallaser scanning microscopy. RNA transcripts and components of the splicing machinery were found to be generally excluded from the interior of the territories occupied by the individual chromosomes. Based on these findings we present a model for the functional compartmentalization of the cell nucleus. According to this model the space between chromosome domains, including the surface areas of these domains, defines a three-dimensional networklike compartment, termed the interchromosome domain (ICO) compartment, in wh ich transcription and splicing of mRNA occurs.

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Section: Probesmentioning

confidence: 99%

Evidence for a nuclear compartment of transcription and splicing located at chromosome domain boundaries

et al. 1993

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“…The high risk, but not the low risk, HPVs transcribe their E6 and E7 genes as linear bicistronic and spliced polycistronic transcripts (Schwarz et al, 1985;Schneider-GaÈ dicke and Schwarz, 1986;Smotkin and Wettstein, 1986). In infected keratinocytes and some celllines derived from HPV-containing cervical tumours, these spliced transcripts are more abundant than nonspliced, to the point that unspliced transcripts are di cult to detect (Doorbar et al, 1990;BoÈ hm et al, 1993;Grassmann et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

HPV-18 E6*I protein modulates the E6-directed degradation of p53 by binding to full-length HPV-18 E6

Pim

Banks

1999

Oncogene

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We have previously demonstrated that ectopic expression of the HPV-18 E6*I protein has an antiproliferative e ect in cells derived from HPV-containing cervical tumours. This e ect correlated with the ability of E6*I to inhibit the E6-mediated degradation of p53 both in vitro and in vivo and with an increase in p53 transcriptional trans-activation. The observation that the E6*I protein can interact with both full-length HPV-18 E6 and E6-AP proteins in vitro indicated the mechanism by which this activity was mediated. In this study we describe a mutational strategy to attempt to di erentiate between the E6-AP and full-length HPV-18 E6 interactions, with respect to the biological function of E6*I. We identify regions of the E6*I protein essential for its interaction with full-length E6 and important for its interaction with E6-AP. We show that a mutant of E6*I which is unable to bind to full-length HPV-18 E6 protein is unable to inhibit the E6-directed degradation of p53 and is also unable to inhibit the proliferation of a cervical tumour-derived cell line. Finally, we show that inhibition of transformed cell growth by E6*I protein correlates with its ability to induce apoptosis in a p53-dependent manner. These results raise the intriguing possibility of using E6*I as a basis for therapeutic intervention in HPV-associated tumours.

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“…9 The presence of splice sites within the E6 ORF, giving rise to the E6*I/E7 transcript, is considered a biological feature of HR-HPV, but not low-risk types (LR-HPV). 8,10 E6*I splice sites have been described for all 12 HR- [11][12][13][14][15][16] and for pHR-HPV types 66 and 68. 16 For the maintenance of the transformed phenotype of HPV-infected CxCa cells continuous expression of both E6 and E7 genes is required.…”

mentioning

confidence: 99%

Biological activity of probable/possible high‐risk human papillomavirus types in cervical cancer

Halec

Schmitt

Dondog

et al. 2012

Intl Journal of Cancer

116

155

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Judging the carcinogenicity of human papillomavirus (HPV) types rarely found in cervical cancer (CxCa) is hindered by lack of studies of their biological activity in cancer tissues. To asses transcriptional activity of HPV types, we have developed ultrashort amplimer, splice-site specific, E6*I mRNA RT-PCR assays for 12 high-risk (HR)-HPV (IARC Group 1) and eight probable/ possible high-risk (pHR)-HPV types (IARC Group 2A/B carcinogens). Previously unreported E6*I splice sites of the six pHR-HPV types 26, 53, 67, 70, 73 and 82 were identified by cloning and sequencing. We analyzed 97 formalin-fixed paraffin-embedded (FFPE) Mongolian CxCa biopsies for presence of HPV DNA by two sensitive genotyping assays, for E6*I transcripts of all HR-/ pHR-HPV types identified and for expression of HPV surrogate markers p16 INK4a , pRb and p53. E6*I of at least one HR-/pHR-HPV was expressed in 94 (98%) of cancer tissues including seven with pHR-HPV types 26, 66, 70 or 82 as single transcribed types. Fifty-eight of E6*I mRNA transcribing cases were analyzable by immunohistochemistry and displayed p16 INK4a overexpression in 57 (98%), pRb downregulation in 56 (97%) and p53 downregulation in 36 (62%) tissues. The newly developed E6*I mRNA RT-PCR assays appeared to be highly sensitive method to analyze HPV transcription in FFPE materials. Our finding of viral oncogene transcription of pHR-HPV types 26, 66, 70 and 82 in cervical tumors, in the absence of any other transcriptionally active HR-type and with p16 INK4a overexpression and pRb downregulation, may support a reassessment of the carcinogenicity classification of these pHR-HPV types.Human papillomaviruses (HPV) with currently more than 150 types defined are a complex group differing in tropism and carcinogenic potential. Detection of HPV DNA in 99.7% of cervical cancer (CxCa) cases has established HPV as an etiological factor for CxCa development. 1,2 Epidemiological studies have demonstrated that 20 mucosal HPV types from five phylogenetically related species of the genus alpha (a5, a6, a7, a9 and a11-termed as ''high-risk clade'') are consistently found as single HPV infections in CxCa worldwide. [3][4][5][6] Based on their frequency in CxCa and available biological data, 12 of these types, i.e., types 16,18,31,33,35,39, 45, 51, 52, 56, 58 and 59 have been defined as carcinogens (IARC Group 1A)-hereafter referred to as high-risk (HR)-HPV. For eight other types, in the high-risk clade, i.e., types 26, 53, 66, 67, 68, 70, 73 and 82, the combination of their low frequency, lack of data on their active transcription and their transforming potential in model systems, has led them to be classified as only probable/possible carcinogens (IARC Groups 2A and 2B)-hereafter referred to as possible highrisk (pHR)-HPV types. 7 In the era of HPV-based cervical cancer precursor screening and of type-specific HPV vaccination, understanding the oncogenic properties of individual

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Different human cervical carcinoma cell lines show similar transcription patterns of human papillomavirus type 18 early genes.

Cited by 416 publications

References 37 publications

Evidence for a nuclear compartment of transcription and splicing located at chromosome domain boundaries

Evidence for a nuclear compartment of transcription and splicing located at chromosome domain boundaries

HPV-18 E6*I protein modulates the E6-directed degradation of p53 by binding to full-length HPV-18 E6

Biological activity of probable/possible high‐risk human papillomavirus types in cervical cancer

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