Cancer control and prevention

Verma, Mukesh

doi:10.1097/mco.0b013e328361dc70

Cited by 33 publications

(7 citation statements)

References 120 publications

(39 reference statements)

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“…Investigate the factors that relate to carcinogenesis may contribute to strategies for cancer treatment and prevention [ 25 ]. As epigenetic aberrations occur and initiate events in tumorigenic processes, epigenetic treatment is a promising strategy for cancer prevention [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

3,6-Dihydroxyflavone regulates microRNA-34a through DNA methylation

Peng

Chang²,

Chen³

et al. 2017

BMC Cancer

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BackgroundBreast cancer is the common cancer in China. In previous study, we determined that 3,6-dihydroxyflavone (3,6-DHF) increases miR-34a significantly in breast carcinogenesis, but the mechanism remains unclear.MethodsWe used qRT-PCR to analyze miR-34a and ten-eleven translocation (TET)1, TET2, TET3 levels in breast cancer cells. With a cellular breast carcinogenesis model and an experimental model of carcinogenesis in rats, TET1 levels were evaluated by western blot analysis and immunofluorescence. TET1 and 5hmC (5-hydroxymethylcytosine) levels were evaluated by immunofluorescence in nude mouse xenografts of MDA-MB-231 cells. Chromatin immunoprecipitation(ChIP) assayed for TET1 on the TET1 promoter, and dot blot analysis of DNA 5hmC was performed in MDA-MB-231 cells. We evaluated the mechanism of 3,6-DHF on the expression of tumor suppressor miR-34a by transfecting them with DNA methyltransferase (DNMT)1 plasmid and TET1 siRNA in breast cancer cells. Methylation-specific PCR detected methylation of the miR-34a promoter.ResultsFirst, we found that 3,6-DHF promotes the expression of TET1 during carcinogen-induced breast carcinogenesis in MCF10A cells and in rats. 3,6-DHF also increased TET1 and 5hmC levels in MDA-MB-231 cells. Further study indicated that TET1 siRNA and pcDNA3/Myc-DNMT1 inhibited the 3,6-DHF reactivation effect on expression of miR-34a in breast cancer cells. Methylation-specific PCR assays indicated that TET1 siRNA and pcDNA3/Myc-DNMT1 inhibit the effect of 3,6-DHF on the demethylation of the miR-34a promoter.ConclusionsOur study showed that 3,6-DHF effectively increases TET1 expression by inhibiting DNMT1 and DNA hypermethylation, and consequently up-regulates miR-34a in breast carcinogenesis.

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Section: Discussionmentioning

confidence: 99%

3,6-Dihydroxyflavone regulates microRNA-34a through DNA methylation

Peng

Chang²,

Chen³

et al. 2017

BMC Cancer

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“…However, emerging evidence indicates that cancer can occur without a change in the nucleotide sequence, through so-called epigenetic alterations. In fact, a combinational crosstalk between genetic and epigenetic alterations has been observed in cancer development, progression, and recurrence [ 32 ]. Both gene mutations and epigenetic alterations can be caused by exposure to various environmental factors, such as dietary components, smoke, and chemicals.…”

Section: Epigenetics and Cancermentioning

confidence: 99%

“…Epigenetic dysregulation, such as increased activity of histone deacetyltransferases (HDACs) and DNA methyltransferases (DNMTs) and changes in noncoding RNA expression, may lead to alterations in the transcription and expression of genes involved in the regulation of cell proliferation and differentiation, cell cycle, and apoptosis [ 32 – 37 ]. The present studies indicated that the level of HDAC5 expression was increased in human glioma and hepatocellular carcinoma, which promoted the proliferation of tumor cells via upregulating Six 1 (Sineoculis homeobox homolog 1) and Notch 1, respectively [ 38 , 39 ].…”

Section: Epigenetics and Cancermentioning

confidence: 99%

Anticancer Activity of Sulforaphane: The Epigenetic Mechanisms and the Nrf2 Signaling Pathway

Jiang

Meng

et al. 2018

Oxidative Medicine and Cellular Longevity

113

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Sulforaphane (SFN), a compound derived from cruciferous vegetables that has been shown to be safe and nontoxic, with minimal/no side effects, has been extensively studied due to its numerous bioactivities, such as anticancer and antioxidant activities. SFN exerts its anticancer effects by modulating key signaling pathways and genes involved in the induction of apoptosis, cell cycle arrest, and inhibition of angiogenesis. SFN also upregulates a series of cytoprotective genes by activating nuclear factor erythroid-2- (NF-E2-) related factor 2 (Nrf2), a critical transcription factor activated in response to oxidative stress; Nrf2 activation is also involved in the cancer-preventive effects of SFN. Accumulating evidence supports that epigenetic modification is an important factor in carcinogenesis and cancer progression, as epigenetic alterations often contribute to the inhibition of tumor-suppressor genes and the activation of oncogenes, which enables cells to acquire cancer-promoting properties. Studies on the mechanisms underlying the anticancer effects of SFN have shown that SFN can reverse such epigenetic alterations in cancers by targeting DNA methyltransferases (DNMTs), histone deacetyltransferases (HDACs), and noncoding RNAs. Therefore, in this review, we will discuss the anticancer activities of SFN and its mechanisms, with a particular emphasis on epigenetic modifications, including epigenetic reactivation of Nrf2.

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“…As we all known, diet is a major aspect of the environment may influence DNA methylation [ 13 ] and especially interesting are nutrients, which are needed for nucleic acid and DNA synthesis and for the enzymes regulating their syntheses, for example, essential amino acids, zinc, vitamins, and so on [ 14 , 15 ]. One of most strongly implicated nutrients is folate, which is a generic term for a naturally occurring family of B-group vitamins composed of an aromatic pteridine ring linked to p-aminobenzoic acid and a glutamate residue B-6 and B-12 [ 3 , 16 ].…”

Section: Introductionmentioning

confidence: 99%

DNA hypomethylation of CBS promoter induced by folate deficiency is a potential noninvasive circulating biomarker for colorectal adenocarcinomas

Geng

Pan

et al. 2017

Oncotarget

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Aberrant DNA methylation patterns, which induced by folate deficiency, play important roles in tumorigenesis of colorectal cancer (CRC). Some DNA methylation alterations can also be detected in cell-free DNA (cfDNA) of patients’ plasma, making cfDNA an ideal noninvasive circulating biomarker. However, exact DNA methylation alterations induced by folate deficiency in tumorigenesis of CRC and exact potential circulating cfDNA methylation biomarker are still unclear. Therefore, DNA methylation patterns of the normal human colon mucosal epithelial cell line (NCM460), cultured with normal or low folate content, were screened and the DNA hypomethylation of cystathionine-beta-synthase (CBS) promoter was further validated in vitro and vivo. Then, the correlation analysis between folate level, DNA methylation alteration in promoter and expression of CBS was carried out in vitro and vivo. Further, the methylation patterns of CBS promoter in plasma cfDNA were detected and statistically correlated with pathological parameters and clinical outcome. Our study showed that DNA hypomethylation in CBS promoter, induced by folate deficiency, would lead to up-regulation of CBS both in vitro and vivo. Patients with cfDNA hypomethylation of CBS promoter in plasma were correlated with high tumor stage and poor clinical outcome. In addition, cfDNA hypomethylation of CBS promoter in plasma was shown to be an independent prognostic factor for recurrence and cancer-related death in CRC. Our results indicated that DNA hypomethylation of CBS promoter induced by folate deficiency could serve as a potential noninvasive circulating biomarker and may be helpful in developing more effective prognostic markers for CRC.

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Cancer control and prevention

Abstract: Natural foods and bioactive food components have characteristics and functions that are similar to epigenetic inhibitors and therefore have potential in cancer control and prevention.

Cited by 33 publications

References 120 publications

3,6-Dihydroxyflavone regulates microRNA-34a through DNA methylation

3,6-Dihydroxyflavone regulates microRNA-34a through DNA methylation

Anticancer Activity of Sulforaphane: The Epigenetic Mechanisms and the Nrf2 Signaling Pathway

DNA hypomethylation of CBS promoter induced by folate deficiency is a potential noninvasive circulating biomarker for colorectal adenocarcinomas

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