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ABSTRACT: Characterization of a Methylation Pattern for Proliferative Verrucous Leukoplakia

PROVIDER: PRJNA663424 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12640646.fastq.gz	Fastqsanger.gz
	SRR12640647.fastq.gz	Fastqsanger.gz
	SRR12640648.fastq.gz	Fastqsanger.gz
	SRR12640649.fastq.gz	Fastqsanger.gz
	SRR12640650.fastq.gz	Fastqsanger.gz

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Epigenome analysis of samples from oral cancer and oral leukoplakias patients

Project description:Genome wide DNA methylation profiling in oral cancer and oral leukoplakia patients. The cohort included 48 patients in total, with control, oral leukoplakia patients and oral cancer patients. The Infinium MethylationEPIC BeadChips 850K has been used to interrogate DNA methylation changes.

2022-09-30 | E-MTAB-12202 | biostudies-arrayexpress

Genome-wide DNA methylation analysis of leukoplakia and oral cancers

Project description:Genomewide DNA methylation profiling of oral leukoplakia and oral sqamous cell carcinoma (OSCC) was performed to delineate candidate gene associated with progression and clinicopathological parameters. All tissue samples were collected after obtaining written informed consent. The DNA methylation profile of 74 OSCC and 22 leukoplakia were compared with 22 normal control tissues from healthy donor.

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Single-cell Transcriptomics Dissects Premalignant Progression in Proliferative Verrucous Leukoplakia

Project description:Proliferative verrucous leukoplakia (PVL) is a potentially malignant disorder characterized by contiguous spread, a spectrum of clinicopathological features and high malignant transformation risk. Despite many efforts to describe the clinicopathological features of PVL progression, so far, there is still a lack of knowledge on the dynamic changes in molecular signature during this process. Hence, we applied single-cell RNA sequencing to 3 biopsy samples from a large PVL lesion. These samples exhibited the histopathological continuum of PVL lesions progression. By analysis for transcriptome profiling of 27,611 cells from these samples, we identified 10 major cell lineages and revealed the cellular remodeling occurring in the progression of PVL lesions, including epithelial, stromal and immune cells. The epithelial cells are shifted to pro-tumorigenic transcriptional cell states and secretory patterns at premalignant stage. Immune cells showed growing immunosuppressive phenotypes during PVL progression. Remarkably, two novel cell subtypes INSR+ endothelial cells and ASPN+ fibroblasts were discovered and may play a vital role in microenvironment remodeling, such as angiogenesis and stromal fibrosis, closely involved in the malignant transformation. Our work preliminarily describes the dynamic molecular properties of PVL lesions, enhances the systematic understanding of the premalignant evolution of PVL and attempts to provide the framework for future research.

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Expression of m6A methylation-modified circRNA in malignant transformation of oral leukoplakia tissue

Project description:Objective This study aimed to investigate the expression and clinical significance of N6-methyladenosine (m6A) modification of circular RNA (circRNA) in oral leukoplakia (OLK) and oral squamous carcinoma cell (OSCC) tissues. Methods Using methylation RNA immunoprecipitation high-throughput sequencing technology (MeRIP-seq) and RNA high-throughput sequencing technology (RNA-seq), the first circRNA transcriptome analysis for detecting m6A methylationome profiles in OLK and OSCC tissues was obtained, followed by bioinformatics analysis. The qRT-PCR technique and protein immunoblotting technique were used to detect the expression of m6A methylesterase in OLK versus OSCC tissues. Results In this study, 275 differential m6A methylation peaks were identified in OLK and OSCC, among which 193 peaks were up-regulated and 82 were down-regulated. Additionally, 198 differential m6A methylation modified circRNAs were observed, with 127 up-regulated and 71 down-regulated (FC ≥ 2, P < 0.05). Most of the identified circRNAs that underwent m6A methylation alterations were derived from overlapping regions. It was found that the differential expression of circRNAs was not correlated with the joint analysis of significantly different m6A-circRNAs between the two groups. Furthermore, downregulation of mETTL14 and FTO protein levels was observed in OSCC tissues, although there were no discernible alterations in RNA levels. Conclusion Our study suggests that m6A methylation modification of circRNA may play a role in the development of oral leukoplakia, and that METTL14 and FTO may be important methylation enzymes that influence the development of oral leukoplakia. These findings may open up new research directions for in-depth investigations to clarify the molecular mechanisms of OLK carcinogenesis.

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