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Experimental study on anti-neoplastic activity of epigallocatechin-3-gallate to digestive tract carcinomas
Zhi-hua Ran1, Jian Zou, Shu-dong Xiao
1Shanghai Institute of Digestive Diseases, Renji Hospital, Shanghai Second Medical University, Shanghai 200001, China. z-ran@online.sh.cn
Background:
Epigallocatechin-3-gallate (EGCG) has been demonstrated to have anti-neoplastic activity, but the effective concentration of EGCG and its possible mechanisms are uncertain. The study on the killing effects of EGCG on different digestive tract cancer cell lines can find target sites of its anti-neoplastic effect and provide a theoretical basis for its clinical application in the treatment of cancers.
Methods:
Methyl thiazolyl tetrazolium (MTT) analysis was made to detect the differential sensitivities of eight digestive tract cancer cell lines to EGCG. The effect of EGCG on cell cycle distribution of sensitive cancer cell line was measured by flow cytometry. By polymerase chain reaction (PCR)-enzyme linked immunosorbent assay (ELISA) protocol, the influence of EGCG on telomerase activity of sensitive cancer cell line was also investigated. RT-PCR method was employed to detect the influence of EGCG on the expressions of hTERT, c-myc, p53 and mad1 genes in sensitive cancer cell line.
Results:
EGCG exhibited dose-dependent killing effects on all eight digestive tract cancer cell lines. The 50% inhibitory concentration (IC50) of SW1116, MKN45, BGC823, SGC7901, AGS, MKN28, HGC27 and LoVo cells were 51.7 micromol/L, 55.9 micromol/L, 68.5 micromol/L, 79.1 micromol/L, 83.8 micromol/L, 119.8 micromol/L, 183.2 micromol/L and 194.6 micromol/L, respectively. There were no apparent changes in cell cycle distribution of sensitive cancer cell line MKN45 48 hours after incubating with three different concentrations of EGCG compared with the controls. It was found that EGCG could suppress the telomerase activity of MKN45 cells, and the effects were dose- and time-dependent. After EGCG administration, the expression of hTERT and c-myc genes in MKN45 cells was decreased, that of the mad1 gene increased, and that of the p53 gene unchanged.
Conclusions:
EGCG has dose-dependent killing effects on different digestive tract cancer cell lines. Administration of EGCG has no obvious effect on cell cycle distribution of sensitive cancer cell line MKN45. The anti-neoplastic activity of EGCG might be due to the inhibition of telomerase activity by means of its influence on hTERT and the up-stream regulation genes.
Insights
Epigallocatechin-3-gallate (EGCG) demonstrates dose-dependent killing effects on digestive tract cancers. Its anti-neoplastic activity may stem from inhibiting telomerase activity and related gene expressions, offering potential for cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Epigallocatechin-3-gallate (EGCG) exhibits anti-neoplastic properties, but its effective concentration and mechanisms require further elucidation.
- Investigating EGCG's effects on digestive tract cancers can identify therapeutic targets and support clinical applications.
Purpose of the Study:
- To evaluate the differential sensitivities of various digestive tract cancer cell lines to EGCG.
- To explore the molecular mechanisms underlying EGCG's anti-cancer effects, including its impact on cell cycle, telomerase activity, and specific gene expressions.
Main Methods:
- Methyl thiazolyl tetrazolium (MTT) assays were used to determine EGCG's inhibitory concentrations (IC50) across eight digestive tract cancer cell lines.
- Flow cytometry assessed EGCG's effect on cell cycle distribution, while PCR-ELISA and RT-PCR investigated its impact on telomerase activity and the expression of hTERT, c-myc, p53, and mad1 genes in sensitive cell lines.
Main Results:
- EGCG displayed dose-dependent cytotoxicity against all eight cancer cell lines, with varying IC50 values.
- No significant alterations in cell cycle distribution were observed in the sensitive MKN45 cell line after EGCG treatment.
- EGCG suppressed telomerase activity in MKN45 cells in a dose- and time-dependent manner, decreasing hTERT and c-myc expression while increasing mad1 expression, with no change in p53.
Conclusions:
- EGCG exhibits significant dose-dependent killing effects on diverse digestive tract cancer cell lines.
- EGCG's anti-neoplastic action is potentially linked to the inhibition of telomerase activity via modulation of hTERT and associated regulatory genes.
- EGCG does not appear to significantly affect the cell cycle distribution of sensitive digestive tract cancer cells.