Epigenetic regulation of active Chinese herbal components for cancer prevention and treatment: A follow-up review

Huang, Zhiying; Huang, Qiuju; Ji, Liyan; Wang, Ying; Qi, Xiaoxiao; Liu, Liang; Liu, Zhongqiu; Lu, Linlin

doi:10.1016/j.phrs.2016.09.023

Cited by 45 publications

(24 citation statements)

References 177 publications

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“…With the development in pharmacology, the constituents of many Chinese herbal medicines have been separated. Therefore, the mechanisms of Chinese herbal medicines for disease treatment have gradually become clear, and in recent years an increasing number of studies have applied Chinese herbal medicine in the treatment of cancer . Therefore, this study explored the effects of the herbal medicine E. prostrata extract (EPE) on oral cancer.…”

Section: Discussionmentioning

confidence: 99%

Antimetastatic effects of Eclipta prostrata extract on oral cancer cells

Liao

Chuang

Hsieh

et al. 2018

Environmental Toxicology

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Eclipta prostrata, a traditional Chinese medication, has been used for the treatment of several diseases. However, the molecular mechanism underlying the effects of Eclipta prostrata extracts (EPE) on human oral cancer cell metastasis remains unclear. We thus examined the effects of EPE on metastasis promoting proteins in oral cancer. Our results revealed that the EPE attenuated SCC-9, HSC-3, and TW2.6 cell migration and invasiveness by reducing matrix metalloproteinase (MMP)-2 enzyme activities. In addition, Western blot analysis revealed that EPE significantly reduced the levels of phosphorylated extracellular signal-regulated kinase 1/2 (ERK 1/2) but not those of c-Jun N-terminal kinase (JNK) 1/2 and p38. In conclusion, we found that EPE could inhibit oral cancer metastasis through the inhibition of MMP-2 expression. Therefore, EPE may be used to prevent the metastasis of oral cancer, and has the potential to be applied to cancer treatment.

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Section: Discussionmentioning

confidence: 99%

Antimetastatic effects of Eclipta prostrata extract on oral cancer cells

Liao

Chuang

Hsieh

et al. 2018

Environmental Toxicology

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“…Therefore, DNMTs are promising therapeutic targets (39). A number of nutritional compounds, including apigenin, genistein, curcumin, sulforaphane, epigallocatechin gallate and Res, regulate cellular epigenetic events, including DNMT activity, in breast, colon, lung and prostate cancer cells (40)(41)(42)(43). Res decreases DNMT enzymatic activity and mRNA levels of DNMT1, DNMT3A and DNMT3B in HCC1806 breast cancer cells (44).…”

Section: Discussionmentioning

confidence: 99%

Resveratrol epigenetically regulates the expression of zinc�finger protein�36 in non‑small cell lung cancer cell lines

et al. 2018

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Zinc finger protein 36 (ZFP36) is an AU-rich element protein that binds to 3'-untranslated regions and promotes the decay of target mRNAs. Downregulation of ZFP36 expression in turn results in stabilization of target mRNAs. A recent study indicated that downregulation of ZFP36 expression in human liver cancer is caused by epigenetic mechanisms. The purpose of the present study was to investigate the potential of resveratrol (Res) to induce ZFP36 expression. Promoter methylation was analyzed using methylation-sensitive restriction analysis. It was determined that Res treatment increased ZFP36 expression and decreased the mRNA levels of ZFP36 target genes in A549 lung cancer cells. Additionally, Res suppressed the expression of DNA (cytosine-5)-methyltransferase 1 and induced demethylation of the ZFP36 promoter. Collectively, the present results demonstrated that Res has anticancer activity through its epigenetic regulation of ZFP36 in non-small cell lung cancer.

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“…Therefore, in this study, we determined whether TFA could attenuate atherosclerosis and attempt to uncover the underlying mechanism. Intriguingly, previous studies have shown that avone can exert protective effect by modulating miRNAs expression in different model of disease [30][31][32][33][34]. Given the important role of miR-33 in cholesterol metabolism and in ammation, and the key role of NF-κB pathway in in ammation, we further determined whether TFA could inhibit atherosclerosis through regulating miR-33 expression and NF-κB pathway.…”

Section: Introductionmentioning

confidence: 94%

Astragalus flavone ameliorates atherosclerosis and hepatic steatosis via improving lipid metabolism and inhibition of inflammation in apoE-/- mice

Zhang

Yang

et al. 2020

Preprint

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Background: Atherosclerosis is a major pathogenic factor in cardiovascular diseases during the aging process. Foam cell formation and endothelial dysfunction play a key role in the initiation and development of atherosclerosis, which are affected by lipid disorder and inflammation. Therefore, the drug for inhibition of endothelial dysfunction and the subsequent foam cell formation is a therapeutic approach for atherosclerosis treatment. Total flavone of Astragalus membranaceus (TFA) is extracted from Astragalus membranaceus that has protective effect on cardiovascular disease. However, the effect of TFA on atherosclerosis and the underlying mechanism remains unknown. Methods: In this study, we determined whether TFA could inhibit atherosclerosis; and uncovered the underlying molecular mechanisms. In vivo, apoE deficient mice were treated with TFA contained in high-fat diet for 16 weeks. After treatment, aorta, macrophage and serum samples were collected to determine atherosclerotic lesions, lipid metabolism, and expression of associated genes. Concurrently, we investigated the effect of TFA on monocyte adhesion, foam cell formation, endothelial activation, and macrophage polarization in vitro and in vivo. Results: TFA reduced atherosclerotic plaque size; and enhanced lesion stability by changing the composition of plaque. Moreover, foam cell formation and its accumulation in arterial wall were attenuated by TFA, which might be attributed to improved lipid disorder, reduced inflammation, and decreased monocyte adhesion to endothelial cells. Mechanistically, TFA reduced the expression of scavenger receptor, such as CD36 and SRA; promoted the expression of ATP-binding cassette transporter A1 and G1 (ABCA1/G1). More importantly, TFA reduced the expression of miR-33, a negative regulator of cholesterol efflux as well as positive mediator on inflammation; and concurrently reduced NFkB activity, by which de-repressed ABCA1/G1 activity and inhibited the inflammation. Conclusions: This study demonstrates that TFA can attenuate atherosclerosis via dual inactivation of miR-33 and NFkB signaling pathway and inhibition of scavenger receptors (CD36 and SRA), which suggests that TFA might be a novel therapeutic approach for inhibition of atherosclerosis.

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Epigenetic regulation of active Chinese herbal components for cancer prevention and treatment: A follow-up review

Cited by 45 publications

References 177 publications

Antimetastatic effects of Eclipta prostrata extract on oral cancer cells

Antimetastatic effects of Eclipta prostrata extract on oral cancer cells

Resveratrol epigenetically regulates the expression of zinc�finger protein�36 in non‑small cell lung cancer cell lines

Astragalus flavone ameliorates atherosclerosis and hepatic steatosis via improving lipid metabolism and inhibition of inflammation in apoE-/- mice

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