OBJECTIVE: To investigate the effect of the major tea polyphenol, (-)-epigallocatechin gallate (EGCG) in cervical carcinogenesis. METHODS: Cell growth rate was examined after treatment for 4, 7, and 10 days with 0-100 microM EGCG in primary human endocervical cells (HEN), human papillomavirus type 18 (HPV 18)-immortalized endocervical cell (HEN-18), ectocervical cell (HEC-18), serum-adapted HEN-18 (HEN-18S), transformed HEC-18 (HEN-18T), and four cervical cancer cell lines. The effect of EGCG treatment was examined on dysplastic epithelium formation in organotypic culture, induction of apoptosis by DNA ladder assay and telomerase activity by PCR telomere extension assay. RESULTS: EGCG inhibited growth more than 90% in HEN-18 and HEC-18, whereas growth inhibition was less in ME180, TMCC-1, HeLa, SiHa, HEC-18T, and HEN-18S. In organotypic culture, thickness of epithelial multilayers was decreased in all EGCG-treated cells. EGCG resulted in apoptosis of HEN-18 or HEC-18, but not HEN-18S nor HEC-18T and inhibited telomerase activity in HEN-18 and HEC-18, as well as HEN-18S and HEC-18T. CONCLUSION: Our data suggest that EGCG prevents the carcinogenesis of cervical cancer, induces apoptosis and inhibited telomerase activity. The effect by EGCG treatment may be associated with the induction of apoptosis and telomerase inhibition in early cervical lesions.
OBJECTIVE: To investigate the effect of the major tea polyphenol, (-)-epigallocatechin gallate (EGCG) in cervical carcinogenesis. METHODS: Cell growth rate was examined after treatment for 4, 7, and 10 days with 0-100 microM EGCG in primary human endocervical cells (HEN), human papillomavirus type 18 (HPV 18)-immortalized endocervical cell (HEN-18), ectocervical cell (HEC-18), serum-adapted HEN-18 (HEN-18S), transformed HEC-18 (HEN-18T), and four cervical cancer cell lines. The effect of EGCG treatment was examined on dysplastic epithelium formation in organotypic culture, induction of apoptosis by DNA ladder assay and telomerase activity by PCR telomere extension assay. RESULTS:EGCG inhibited growth more than 90% in HEN-18 and HEC-18, whereas growth inhibition was less in ME180, TMCC-1, HeLa, SiHa, HEC-18T, and HEN-18S. In organotypic culture, thickness of epithelial multilayers was decreased in all EGCG-treated cells. EGCG resulted in apoptosis of HEN-18 or HEC-18, but not HEN-18S nor HEC-18T and inhibited telomerase activity in HEN-18 and HEC-18, as well as HEN-18S and HEC-18T. CONCLUSION: Our data suggest that EGCG prevents the carcinogenesis of cervical cancer, induces apoptosis and inhibited telomerase activity. The effect by EGCG treatment may be associated with the induction of apoptosis and telomerase inhibition in early cervical lesions.
Authors: Changping Zou; Huaguang Liu; Jean M Feugang; Zhengping Hao; H-H Sherry Chow; Francisco Garcia Journal: Int J Gynecol Cancer Date: 2010-05 Impact factor: 3.437
Authors: Francisco A R Garcia; Terri Cornelison; Tomas Nuño; David L Greenspan; John W Byron; Chiu-Hsieh Hsu; David S Alberts; H-H Sherry Chow Journal: Gynecol Oncol Date: 2014-01-02 Impact factor: 5.482