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Folate deficiency and repletion affects DNA stability and cellular growth of HPV16-immortalized human keratinocytes

ABSTRACT: Folate deficiency and repletion affects DNA stability and cellular growth of HPV16-immortalized human keratinocytes

PROVIDER: PRJEB25728 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2608100_1.fastq.gz	Fastqsanger.gz
	ERR2608100_2.fastq.gz	Fastqsanger.gz
	ERR2608101_1.fastq.gz	Fastqsanger.gz
	ERR2608101_2.fastq.gz	Fastqsanger.gz

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Folate modulation induces chromosomal instability and higher proliferation of immortalized human keratinocytes

Project description:Gene expression variation upon folate deficiency and repletion in human foreskin keratinocytes immortalized by HPV16E6E7

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Project description:The overexpression of Six1, a member of the Six family of homeodomain transcription factors, has been found in various human cancers, and is associated with tumor progression and metastasis. We previously determined that the expression of Six1 mRNA increased during in vitro progression of human papillomavirus type 16 (HPV16)-immortalized human keratinocytes (HKc/HPV16) toward a differentiation-resistant (HKc/DR) phenotype. However, if Six1 promotes HPV16-mediated transformation or not remains unknown. HKc/DR were transfected with a Six1 or control vector and RNA isolated from these cells were used in an Agilent two-color gene expression profiling experiment. The goal was to determine the effects of Six1 on global gene expression.

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Gene expression of cervical cells and immortalized keratinocytes transfected with whole genomes of HPV16 and HPV18

Project description:Human ectocervical and endocervical cells immortalized by HPV16 E6/E7 (designated as Ect and End, respectively) and normal human immortalized keratinocytes (NIKS), were transfected with whole genomes of HPV16 or HPV18, and were subsequently grown in standard monolayer culture until passage 2. Total RNAs were extracted and subjected to TORAY 3D-gene analysis service using the 3D-Gene Human Oligo chip 25K (TORAY, Tokyo, Japan).

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Dietary folate depletion and repletion

Project description:This SuperSeries is composed of the following subset Series: GSE9242: Dietary folate depletion and repletion in A/J and C57BL/6J mice GSE9243: Dietary folate depletion and repletion in C57BL/6J mice, ApoE knockout mice, and choline supplemented C57BL/6J mice Keywords: SuperSeries Refer to individual Series

2010-06-20 | E-GEOD-9245 | biostudies-arrayexpress

Analysis of HPV16 E2 host gene expression using TERT immortalized keratinocytes (NOKs) cell lines and RNA-sequencing

Project description:HPV must reprogram host gene expression to promote infection, and HPV proteins E6 and E7 contribute to this via targeting of cellular transcription factors including p53 and pRb respectively. The HPV16 E2 protein regulated host gene expression in U2OS cells and in this study we extend these observations into NOKs that are capable of suporting late stages of the HPV16 life cycle. We observed repression of innate immune genes by E2 that are also repressed by the intact HPV16 genome in NOKs. There was a highly significant overlap of the E2 regulated genes with those regulated by the intact HPV16 genome in the same cell type. siRNA targeting of E2 reversed repression of E2 targed genes. The ability of E2 to repress innate immune genes was confirmed in an ano-genital immortalized keratinocyte cell line, N/Tert-1.

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Impact of HPV16 E6 and E7 oncogenes together with Chlamydia trachomatis infection on proteome changes in immortalized oral keratinocytes

Project description:Certain types of Human papilloma viruses (HPV) are the etiological agents for cervical cancer. However, not all infections of high-risk HPVs will finally lead to cancer since most HPV infections are cleared without any consequences. Chlamydia trachomatis is the most prevalent sexual transmitted bacteria and is an obligatory intracellular pathogen exhibiting tropism in endocervical epithelial cells. Over the past decades, C. trachomatis is thought to be a potential co-factor for cervical cancer formation, but there are also studies that did not show such a correlation. To address this question in molecular terms, we stably expressed HPV16 E6 and E7 in spontaneously immortalized NOKs (normal oral keratinocytes) and performed SILAC (stable isotope labeling by amino acids in cell culture) with or without C. trachomatis infection to study the impact of HPV16 oncogene expression and C. trachomatis infection on host proteome changes.

2019-03-18 | PXD012186 | Pride

Transcriptome of human keratinocytes with or without HPV16 oncogene expression

Project description:We used freshly established immortalized human keratinocytes with a well-defined HPV16 E6 E7 expression cassette to get a more complete and less biased overview about global changes induced by HPV16 using RNA-seq. We identified novel factors regulated by HPV oncogenes that could serve an essential role in cancer development.

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Folate Repletion after Deficiency Induces Irreversible Genomic and Transcriptional Changes in Human Papillomavirus Type 16 (HPV16)-Immortalized Human Keratinocytes.

Project description:Supplementation of micronutrients like folate is a double-edged sword in terms of their ambivalent role in cell metabolism. Although several epidemiological studies support a protective role of folate in carcinogenesis, there are also data arguing for an opposite effect. To address this issue in the context of human papillomavirus (HPV)-induced transformation, the molecular events of different folate availability on human keratinocytes immortalized by HPV16 E6 and E7 oncoproteins were examined. Several sublines were established: Control (4.5 µM folate), folate deficient (0.002 µM folate), and repleted cells (4.5 µM folate). Cells were analyzed in terms of oncogene expression, DNA damage and repair, karyotype changes, whole-genome sequencing, and transcriptomics. Here we show that folate depletion irreversibly induces DNA damage, impairment of DNA repair fidelity, and unique chromosomal alterations. Repleted cells additionally underwent growth advantage and enhanced clonogenicity, while the above mentioned impaired molecular properties became even more pronounced. Overall, it appears that a period of folate deficiency followed by repletion can shape immortalized cells toward an anomalous phenotype, thereby potentially contributing to carcinogenesis. These observations should elicit questions and inquiries for broader additional studies regarding folate fortification programs, especially in developing countries with micronutrient deficiencies and high HPV prevalence.

| S-EPMC6429418 | biostudies-literature

Gene expression of cervical cells and immortalized keratinocytes transfected with whole genomes of HPV16 and HPV18

Project description:Gene expression of cervical cells and immortalized keratinocytes transfected with whole genomes of HPV16 and HPV18

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