Tranexamic acid may promote melanocores clustering in keratinocytes through upregulation of Rab5b
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA856499 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20016487_1.fastq.gz | Fastqsanger.gz | |||
| SRR20016487_2.fastq.gz | Fastqsanger.gz | |||
| SRR20016488_1.fastq.gz | Fastqsanger.gz | |||
| SRR20016488_2.fastq.gz | Fastqsanger.gz | |||
| SRR20016489_1.fastq.gz | Fastqsanger.gz |
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Project description:Genome-wide 10k SNP profiling of FOXM1B-transduced N/TERT and primary normal human epidermal keratinocytes (NHEK). The aim of this study was to study the cancer initiation role of UVB and FOXM1B upregulation in NHEK. Upregulation of FOXM1B alone (without UVB) was found to directly induce genomic instability in the form of copy number aberration (CNA) and low levels of loss of heterozygosity (LOH) in primary NHEK. The FOXM1B-induced CNA was found to be retained and accumulated in subsequent cell culture passages. UVB-exposure resulted in significant chromosomal LOH and CNA in N/TERT cells expressing FOXM1B but not in EGFP-expressing cells. This indicates that UVB corroborated with FOXM1B to recruit LOH and CNA which may predispose cell to malignant transformation. Collectively, these results indicate that aberrant upregulation of FOXM1B in skin keratinocytes following UVB exposure may be an early mechanism whereby cells acquire genomic changes required for oncogenesis. Keywords: Genome-wide SNP profiling for loss of heterozygosity (LOH) and copy number aberration (CNA), FOXM1, UVB, Keratinocytes, Basal cell carcinoma, genomic instability, carcinogenesis, squamous cell carcinoma.
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