Human papillomavirus
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Project description:To explore the circRNA expression profiles during the development and progression of cervical cancer, we performed RNA sequencing analysis with ribosomal RNA-depleted in HPV negative normal cervical epithelium, HPV16 positive normal cervical epithelium, HPV16 positive high-grade squamous intraepithelial lesion (HSIL), and HPV16 positive cervical squamous cell carcinoma tissues,6 cases in each group.Totally 66868 circRNAs were identified (Back-spliced junctions reads≥1)
2020-12-21 | GSE147009 | GEO
Project description:The infection with high-risk human papillomavirus is aetiologically linked to cervical cancer, the role of miRNAs regulated by virus oncogene in cancer progression remain largely unknown. Here, we screened the differentially expressed miRNAs with miRNA array between virus oncogene e6/e7 silenced and not in HPV16-positive cervical cancer cell lines
2016-07-01 | GSE68153 | GEO
Project description:Persistent infection by high-risk human papillomaviruses (HPVs) is associated with the development of cervical cancer and a subset of anogenital and head and neck squamous cell carcinomas. Abnormal expression of cellular microRNAs (miRNAs) plays an important role in the development of cancer, including HPV-related tumors. MiRNA expression profile was investigated by microrray analysis in the HPV-positive cervical cancer cell lines SiHa (HPV16-positive cell line derived from a cervical squamous cell carcinoma), CaSki (HPV16-positive cell line derived from a metastatic cervical epidermoid carcinoma), and HeLa (HPV18-positive cell line derived from a cervical adenocarcinoma) and compared with primary HFKs and C33a (HPV-negative cervical cell line).
2018-01-16 | E-MTAB-6361 | biostudies-arrayexpress
Project description:The infection with high-risk human papillomavirus is aetiologically linked to cervical cancer, the role of miRNAs regulated by virus oncogene in cancer progression remain largely unknown. Here, we screened the differentially expressed miRNAs with miRNA array between virus oncogene e6/e7 silenced and not in HPV16-positive cervical cancer cell lines In the study, we screened the differentially expressed miRNAs with miRNA array (Exiqon, miRCURY LNA microRNA array, 7th gen [hsa, miRBase 18]) between virus oncogene e6/e7 silenced and not in HPV16-positive cervical cancer cell lines to found miRNAs regulated by virus oncogene e6/e7. Biological replicates: 3 control, 3 e6/e7 silenced, independently grown and harvested. four replicates per array.
2016-07-01 | E-GEOD-68153 | biostudies-arrayexpress
Project description:Background: Cervical cancer, prevalent in low- and middle-income countries, is primarily caused by high-risk HPV16. Vesicle-Associated Membrane Protein 8 (VAMP8), involved in vesicle trafficking and autophagy, may influence HPV16-related cervical cancer progression. Methods: VAMP8 expression was evaluated in cervical tissue specimens from patients with HPV16-positive lesions (including low- and high-grade squamous intraepithelial lesions and cancer) and HPV-negative normal controls using proteomics, qPCR, and immunohistochemistry. A Cox proportional hazards model for prognosis was developed using immunohistochemical data from a cohort of cervical cancer patients. The clinical significance of VAMP8 was further assessed using RNA-seq and clinical data from The Cancer Genome Atlas-Cervical Cancer (TCGA-CESC) cohort. The effects of VAMP8 on autophagy and tumor progression were examined in HPV16 E6/E7-immortalized cervical epithelial cells (Ect1/E6E7) and cervical cancer cell lines (SiHa, HeLa, C-33A) in vitro, and in a SiHa xenograft model in vivo. Transcriptomic analysis of Ect1/E6E7 and SiHa cells identified VAMP8-regulated pathways. Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays in SiHa cells were used to confirm the regulation of the HIF-1 pathway. Results: VAMP8 was upregulated in HPV16-positive samples, particularly in low-grade squamous intraepithelial lesions (LSIL). Elevated VAMP8 correlated with poor survival outcomes and advanced tumor stages. VAMP8 enhanced autophagy and reduced proliferation and invasiveness in HPV16-positive cervical cells but increased in established cancer cell lines. In vivo, VAMP8 overexpression promoted tumor growth and autophagy. The HIF-1 pathway emerged as a key regulatory axis of VAMP8, enhancing hypoxic responses and angiogenesis. Conclusion: Elevated VAMP8 in HPV16-associated cervical cancer promotes tumor progression by enhancing autophagy via the HIF-1 pathway, suggesting its potential as a diagnostic and prognostic biomarker.
2025-08-30 | GSE306495 | 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:Analysis of the E6 and E7 genes of HPV16 isolates from cervical carcinomas in Latvia.
| PRJNA1293798 | ENA
Project description:CircRNAs have been found to regulate mRNA expression levels and serve an important role in cervix carcinogenesis. To explore the circRNA expression profiles during the development and progression of cervical cancer, we performed microarray analysis with total RNA in normal cervical epithelium(n=7), HPV16 positive high-grade squamous intraepithelial lesion (HSIL)(n=6), and HPV16 positive cervical squamous cell carcinoma tissues(n=7).
2021-02-10 | GSE166466 | GEO
Project description:It is well known that high-risk human papilloma virus (HR-HPV) infection is strongly associated with cervical cancer and E7 was identified as one of the key initiators in HPV-mediated carcinogenesis. Here we show that lactate dehydrogenase A (LDHA) preferably locates in the nucleus in HPV16-positive cervical tumors due to E7-induced intracellular reactive oxygen species (ROS) accumulation. Surprisingly, nuclear LDHA gains a non-canonical enzyme activity to produce α-hydroxybutyrate and triggers DOT1L (disruptor of telomeric silencing 1-like)-mediated histone H3K79 hypermethylation, resulting in the activation of antioxidant responses and Wnt signaling pathway. Furthermore, HPV16 E7 knocking-out reduces LDHA nuclear translocation and H3K79 tri-methylation in K14-HPV16 transgenic mouse model. HPV16 E7 level is significantly positively correlated with nuclear LDHA and H3K79 tri-methylation in cervical cancer. Collectively, our findings uncover a non-canonical enzyme activity of nuclear LDHA to epigenetically control cellular redox balance and cell proliferation facilitating HPV-induced cervical cancer development.
2018-09-24 | PXD011058 | Pride
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