English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Open

The purpose of this study was to determine the effect of the FHIT gene on tumorigenesis of cervical cancer. RT-PCR and MTT were used to detect the expression of FHIT and cell proliferation respectively. Flow cytometry was used to test cell cycle and cell apoptosis. The expression of FHIT was not induced at all four cervical cancer cells treated with demethylating agent 5-aza-2'-deoxycytidine (5-Aza-CdR). However, a constant level of FHIT expression was detected in the human umbilical vein endothelial cell before and after 5-aza-dC treatment. The proliferation of all four cervical cancer cells was inhibited evidently when treated with 5-aza-dC and the inhibiting rate of cell growth along with the increasing concentration of 5-aza-dC. There was no obvious inhibiting effect on the growth of the human umbilical vein endothelial cell treated with 5-aza-dC. An increasing G1 phase and high apoptosis rate were detected in all four cervical cancer cells. However, a negligible change was seen in the human umbilical vein endothelial cell. These results suggest that aberrant methylation of the FHIT gene might be a key mechanism for silenced FHIT gene, which could be reactivated and whose tumor suppressing function could be restored by demethylating agent treatment.

Regulation of DNA methylation on the expression of the FHIT gene contributes to cervical carcinoma cell tumorigenesis