Cervical cancer is one of the most common cancers that affects women in Poland. Human Papillomaviruses (mainly HPV16, 18 and 33) -mediated transformation of epithelial cells has been recognized as a multi-step process, in which, apart from the presence of the virus, additional factors are needed.

It has been suggested that TSG101 plays a very important role in tumor formation and progression. TSG101 gene was mapped to chromosome 11 p15.1-p15.2. This region of chromosome is known to be associated with a loss of heterozygosity (LOH) in several tumor types. Although somatic mutations or deletions within the TSG101 gene are rare events, aberrant splicing forms have been observed frequently in a variety of human cancers.

TSG101 encodes a multidomain protein involved in a range of biological functions: ubiquitination, transcriptional regulation, endosomal trafficking, proliferation and cell survival.

Real-Time PCR analysis showed decreased level of TSG101 mRNA in epithelial cells during different stages of cervical cancer development. Reductions of TSG101 mRNA level might be caused by several different factors such as structural changes (point mutations, deletions) in coding or promoter sequences, by promoter hypermethylation or by changes in the profile of transcription factors involved in TSG101 gene expression. Application of PCR/SSCP methods demonstrated, that there is no mutation in TSG101 coding sequence. Preliminary studies of CpG island methylation patterns in TSG101 promoter sequence in neoplasia and cancer cells showed minor alterations in comparision to healthy tissue. These results suggest that decreased level of TSG101 mRNA in epithelial cells during different stages of cervical cancer development is neither regulated by epigenetic modifications nor by mutations in coding sequence.

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