Human papillomavirus 16 strain:16
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ABSTRACT:
PROVIDER: PRJNA1291997 | ENA |
REPOSITORIES: ENA
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Project description:Analysis of the E6 and E7 genes of HPV16 isolates from cervical carcinomas in Latvia.
| PRJNA1293798 | ENA
Project description:Human papillomavirus (HPV) is the etiological agent of cervical cancer. Three viral proteins, E5, E6 and E7 have been implicated in cell transformation. Increased expression of sialic acid and sialylated antigens have been reported during cervix transformation, these results agree with the increased mRNA levels of the sialyltransferases genes ST6GAL1 and ST3GAL3 reported in premalignant and malignant tissue of the cervix. E6 and E7 HPV oncoproteins modify the expression of some glycogenes. The role of E5 HPV oncoprotein in the glycogene expression changes in premalignant and malignant cervical tissue has not been reported. The objective of this work was to identify glycogenes that modify their expression by E5 HPV oncoprotein in HaCaT cell line. A gene expression microarray was performed on HaCaT cells that stably expressed the HPV16 E5 oncogene. Analysis revealed alteration in some glycogenes including upregulation of ST6GAL1 and ST3GAL3. The increased mRNA levels of both genes were confirmed by qRT-PCR. In addition, an in-silico analysis was performed to identify glycosylation networks altered in presence of E5 oncoprotein. The analysis showed that E5 could modify the sialic acid expression, keratan sulfate synthesis, N-glycosylation and biosynthesis of glycosaminoglycans. This is the first report of the role of HPV16 E5 oncoprotein on glycogenes expression changes. Moreover, our results suggest that the increase of the sialyltransferases genes reported in premalignant and malignant cervical tissue, could be the result of the expression of E5 oncoprotein. These results provide information of the possible role of HPV infection on the sialylation changes in the cervical epithelium identified in premalignant lesions and cancer.
2018-08-21 | GSE118776 | GEO
Project description:To investigate the extent of host methylome dysregulation by the human papillomavirus (HPV) oncoprotein E7, we performed methylome array analysis on normal immortalized keratinocytes from skin (NIKS), NIKS cells maintaining the HPV16 or 18 episomes (NIKS-16, NIKS-18, respectively), and NIKS cells maintaining the HPV-16 episome deficient in E7 expression (NIKS-16ΔE7).
2017-06-11 | GSE83261 | GEO
Project description:To investigate the extent of gene expression dysregulation by the human papillomavirus (HPV) oncoprotein E7, we performed global gene expression analysis on normal immortalized keratinocytes from skin (NIKS), NIKS cells maintaining the HPV16 or 18 episomes (NIKS-16, NIKS-18, respectively), and NIKS cells maintaining the HPV-16 episome deficient in E7 expression (NIKS-16ΔE7).
2017-06-11 | GSE83259 | GEO
Project description:Integration of human papillomavirus (HPV) DNA into the host genome is a critical aetiological event in the progression from normal cervix to intraepithelial neoplasm, and finally to invasive cervical cancer. In this study, we want to know how HPV DNA physical status relates to treatment outcome for cervical carcinomas.
2013-07-28 | GSE49288 | GEO
Project description:The effect of human papillomavirus 16 E5 oncogene on cellular gene expression in human epithelial cells was studied.
2011-09-01 | GSE24908 | GEO
Project description:Oncogene expressing human papillomavirus type 16 (HPV16) is found in a subset of head and neck squamous cell carcinomas (HNSCC). HPV16 drives carcinogenesis by inactivating p53 and pRb with the viral oncoproteins E6 and E7, reflected by a low level of mutations in TP53 and allelic loss at 3p, 9p and 17p, genetic changes frequently found in HNSCCs of non-viral etiology. We hypothesize that two pathways to HNSCC exist: one determined by HPV16 and one by environmental carcinogens. To define the critical genetic events in these two pathways, we now present a detailed genome analysis of HNSCC with and without HPV16 involvement by employing high resolution micro-array comparative genomic hybridization. Four regions showed alterations in HPV-negative tumors that were absent in HPV-positive tumors: losses at 3p11.2-26.3, 5q11.2-35.2, 9p21.1-24, and gains/amplifications at 11q12.1-13.4. Also, HPV16-negative tumors demonstrated loss at 18q12.1-23, in contrast to gain in HPV16-positive tumors. Seven regions were altered at high frequency (>33%) in both groups: gains at 3q22.2-qter, 5p15.2-pter, 8p11.2-qter, 9q22-34.1, 20p-20q and losses at 11q14.1-qter and 13q11-33. These data show that HNSCC arising by environmental carcinogens are characterized by genetic alterations that differ from those observed in HPV16-induced HNSCC, and most likely occur early in carcinogenesis. A number of genetic changes are shared in both tumor groups and can be considered crucial in the later stages of HNSCC progression.
2009-05-26 | GSE11931 | GEO
Project description:The effect of human papillomavirus 16 E5 oncogene on cellular gene expression in human epithelial cells was studied. Alterations in cellular gene expression due to human papillomavirus type 16 E5 oncogene were studied in triplicate microarray screens. Epithelial cells where E5 expression was induced for 0, 2, 4, 24, 48, 72 and 96h were compared to control cells.
2011-08-31 | E-GEOD-24908 | biostudies-arrayexpress
Project description:Oncogene expressing human papillomavirus type 16 (HPV16) is found in a subset of head and neck squamous cell carcinomas (HNSCC). HPV16 drives carcinogenesis by inactivating p53 and pRb with the viral oncoproteins E6 and E7, reflected by a low level of mutations in TP53 and allelic loss at 3p, 9p and 17p, genetic changes frequently found in HNSCCs of non-viral etiology. We hypothesize that two pathways to HNSCC exist: one determined by HPV16 and one by environmental carcinogens. To define the critical genetic events in these two pathways, we now present a detailed genome analysis of HNSCC with and without HPV16 involvement by employing high resolution micro-array comparative genomic hybridization. Four regions showed alterations in HPV-negative tumors that were absent in HPV-positive tumors: losses at 3p11.2-26.3, 5q11.2-35.2, 9p21.1-24, and gains/amplifications at 11q12.1-13.4. Also, HPV16-negative tumors demonstrated loss at 18q12.1-23, in contrast to gain in HPV16-positive tumors. Seven regions were altered at high frequency (>33%) in both groups: gains at 3q22.2-qter, 5p15.2-pter, 8p11.2-qter, 9q22-34.1, 20p-20q and losses at 11q14.1-qter and 13q11-33. These data show that HNSCC arising by environmental carcinogens are characterized by genetic alterations that differ from those observed in HPV16-induced HNSCC, and most likely occur early in carcinogenesis. A number of genetic changes are shared in both tumor groups and can be considered crucial in the later stages of HNSCC progression. Tumor DNA is isolated from fresh frozen tissue. Tumor DNA is enriched by microdissection. Reference DNA is isolated from blood of normal individuals of the opposit gender.
2009-05-26 | E-GEOD-11931 | biostudies-arrayexpress