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The study of effect of tea polyphenols on microsatellite instability colorectal cancer and its molecular mechanism
Heiying Jin1, Xuanzhong Tan, Xiufang Liu
1National Center of Colorectal Surgery, The 3rd affiliated Hospital of Nanjing University of Traditional Chinese Medicine, 1 Jinling Road, Jiangsu, 210001, China. jinheiying@yahoo.com.cn
Introduction:
Tea polyphenol has been shown to have anti-colorectal cancer and anti-gene mutation effects, although the mechanism of inhibition of microsatellite instability (MSI) colorectal cancer is not known.
Materials And Methods:
Using LoVo, HCT-116, HT-29, and SW480 cells treated with an aqueous solution of tea polyphenol, cell proliferation was detected by the methyl thiazolyl tetrazolium method, changes in microsatellite sequences by the Genescan method and changes in the gene expression of LoVo cells using Illumina expression arrays.
Results:
The proliferation inhibition rate of LoVo, HCT-116, HT-29, and SW480 cells treated with tea polyphenol increased with increasing drug concentration and showed an increasing tendency with time. The proliferation inhibition rate of LoVo and HCT-116 cells with tea polyphenols was higher than that of HT-29 and SW480 cells, and there was a significant difference in the proliferation inhibition rate at 24, 72 h and 1 week. The microsatellite sequence of LoVo cells treated with tea polyphenols remained stable.
Discussion:
The gene expression arrays and quantitative RT-PCR suggested that tea polyphenol inhibited the gene expression of metallothionein 2A (MT2A), transcription factor (MAFA), hairy and enhancer of split 1 (HES1), and jagged1 (JAG1) nearly twofold over controls. It was also found that tea polyphenol inhibited the BAX and p38 genes with a more than twofold difference but did not significantly inhibited the NFκB pathway.
Conclusion:
Tea polyphenol significantly inhibited the proliferation of MSI colorectal cancer signals maintained stable at the microsatellite state in MSI colorectal cancer. Tea polyphenol inhibited the gene expression of HES1, JAG1, MT2A, and MAFA but upregulated the gene expression of BAX and downregulated that of (P)38. Further research is required to investigate how these pathways are interrelated.
Insights
Tea polyphenol inhibits colorectal cancer cell growth and maintains microsatellite stability. It affects gene expression, downregulating HES1, JAG1, MT2A, and MAFA while upregulating BAX and downregulating p38.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Tea polyphenols exhibit anti-colorectal cancer properties.
- The precise mechanism of tea polyphenol's inhibition of microsatellite instability (MSI) colorectal cancer remains unclear.
Purpose of the Study:
- To investigate the inhibitory effects of tea polyphenol on colorectal cancer cell proliferation.
- To elucidate the molecular mechanisms underlying tea polyphenol's action on MSI colorectal cancer, including gene expression changes.
Main Methods:
- Utilized LoVo, HCT-116, HT-29, and SW480 colorectal cancer cell lines.
- Assessed cell proliferation using the methyl thiazolyl tetrazolium assay.
- Analyzed microsatellite sequence stability with the Genescan method and gene expression profiles via Illumina expression arrays.
Main Results:
- Tea polyphenol demonstrated dose- and time-dependent inhibition of colorectal cancer cell proliferation.
- LoVo and HCT-116 cells showed greater sensitivity to tea polyphenol compared to HT-29 and SW480 cells.
- Microsatellite sequences in LoVo cells remained stable following tea polyphenol treatment.
Conclusions:
- Tea polyphenol significantly inhibits MSI colorectal cancer cell proliferation and maintains microsatellite stability.
- Gene expression analysis revealed tea polyphenol downregulates HES1, JAG1, MT2A, and MAFA, while upregulating BAX and downregulating p38.
- Further investigation is needed to understand the interconnections between these affected pathways.
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