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Apoptotic effect of Polygonum Cuspidatum in oral cancer cells through the regulation of specificity protein 1
1Department of Oral Pathology, School of Dentistry and Institute of Oral Bioscience, BK21 Project, Chonbuk National University, Jeonju, Korea.
Objectives:
The aim of this study was to evaluate the growth inhibitory and apoptosis-inducing effects and mechanisms of Polygonum cuspidatum root in oral cancer cells.
Materials And Methods:
The testing materials were separated by normal-phase silica gel liquid chromatography. The effect of P. cuspidatum root on apoptotsis and its mechanism were performed using 3-(4,5-dimethylthiazol-20yl)-(3-carboxymethoxyphenyl)-2-(4-sulphophenyl)-2H-tetrazolium) (MTS) assay, western blot analysis, RT-PCR, promoter assay, and (4'-6-Diamidino-2-phenylindole) (DAPI) staining.
Results:
The methanol extract of P. cuspidatum (MEPC) inhibited the proliferation of oral cancer cells by inducing caspase-dependent apoptosis. Protein and mRNA expression levels and the transactivation of Specificity protein 1 (Sp1) were markedly decreased in KB cells treated with MEPC. Ethyl acetate fraction (EA) from MEPC was more potent than aqueous fraction (AQ) from MEPC to induce apoptosis. F2, F3, and F4 from EA differentially inhibited the growth of KB cells, and it depends on the amount of Emodin in F2, F3, and F4. Moreover, Emodin inhibited oral cancer cell growth and induced caspase-dependent apoptosis by decreasing Sp1. MEPC also decreased an apoptosis-related downstream target of Sp1 protein, survivin.
Conclusion:
The results from this study strongly suggest that MEPC, its fraction, and Emodin may be potential bioactive materials to cause apoptosis mechanism via the down-regulation of Sp1 in oral cancer cells.
Insights
Polygonum cuspidatum root extract inhibits oral cancer cell growth by inducing apoptosis. This natural compound, particularly Emodin, works by down-regulating Specificity protein 1 (Sp1) signaling pathways.
Area of Science:
- Phytochemistry
- Molecular Biology
- Cancer Research
Background:
- Oral cancer presents a significant global health challenge.
- Identifying novel therapeutic agents from natural sources is crucial for effective treatment.
- Polygonum cuspidatum is a traditional medicinal herb with potential anti-cancer properties.
Purpose of the Study:
- To investigate the anti-cancer effects of Polygonum cuspidatum root extract on oral cancer cells.
- To elucidate the underlying mechanisms of growth inhibition and apoptosis induction.
- To identify key bioactive compounds responsible for these effects.
Main Methods:
- Extraction and fractionation of Polygonum cuspidatum root.
- Cell proliferation assays (MTS assay).
- Apoptosis analysis (Western blot, RT-PCR, DAPI staining, promoter assay).
Main Results:
- Methanol extract of Polygonum cuspidatum (MEPC) inhibited oral cancer cell proliferation via caspase-dependent apoptosis.
- MEPC and its fractions, particularly ethyl acetate fraction (EA) containing Emodin, significantly reduced cell growth.
- Emodin and MEPC decreased Specificity protein 1 (Sp1) expression and its downstream target survivin, inducing apoptosis.
Conclusions:
- Polygonum cuspidatum root extract, its fractions, and Emodin show potential as anti-oral cancer agents.
- The mechanism involves down-regulation of Sp1 signaling, leading to apoptosis.
- Further research into Emodin and Sp1 pathways could yield novel therapeutic strategies for oral cancer.
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