[Epigenetic changes in the promoter of the fragile histidine triad (FHIT) gene in human sebocytes under the influence of in vitro culture].

BACKGROUND

Due to the lack of tumor suppressor function of the fragile histidine triad (FHIT) gene product, sebaceous gland carcinomas can develop.

OBJECTIVE

The model of the sebocyte cell line SZ95 was used to identify methylated CpG islands at the 5'-end of the FHIT gene and the decrease of gene expression as well as the increase of double-stranded (ds) DNA breaks were examined.

MATERIAL AND METHODS

Methylation, immunofluorescence analysis, promotor sequencing and treatment of SZ95 cells with 5‑azacytidine/trichostatin A (TSA).

RESULTS

The cultivation was accompanied by an increasing methylation of the CpG islands, a decrease of the FHIT gene expression and an accumulation of ds-DNA breaks. Treatment with 5‑azacytidine/TSA showed a decrease in DNA methylation and a re-expression of FHIT transcripts.

DISCUSSION

Epigenetic changes in the cellular genome are caused by in vitro cell culture. Consequently, a positive selection of sebocytes with an epigenetically inactivated FHIT locus occurs.