Curcumin reduces the expression of Bcl-2 by upregulating miR-15a and miR-16 in MCF-7 cells

Yang, Jie; Cao, Yunxin; Sun, Jui Sheng; Zhang, Yong

doi:10.1007/s12032-009-9344-3

Cited by 199 publications

(120 citation statements)

References 20 publications

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“…Suppression of miRNA-15a expression significantly reversed the anticancer effect of curcumin on cell viability of AMC-HN-8 cells. Yang et al (28) reported that curcumin upregulated miR-15a and reduced the expression of Bcl-2 in MCF-7 breast cancer cells. Gao et al (29) suggested that curcumin decreases the expression of Wilms' tumor protein through miR-15a and miR-16-1 in leukemic cells.…”

Section: Discussionmentioning

confidence: 99%

Curcumin inhibits cell proliferation and promotes apoptosis of laryngeal cancer cells through Bcl-2 and PI3K/Akt, and by upregulating miR-15a

Mou

Zhang

et al. 2017

Oncology Letters

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Abstract. Curcumin is a natural compound extracted from the dried rhizomes of Curcuma (curcuma root or zedoary) that exhibits extensive pharmacological effects and low toxicity. The aim of the present study was to investigate whether curcumin inhibits cell proliferation and promotes apoptosis of laryngeal cancer through Bcl-2 and phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), and by upregulating microRNA-15a (miR-15a). It was demonstrated that curcumin inhibits cell proliferation, and promotes apoptosis and increased caspase-3 activity of human laryngeal cancer cells. Furthermore, curcumin decreased Bcl-2 and PI3K protein expression, and decreased the phospho (p)-Akt protein expression of human laryngeal cancer cells. Furthermore, curcumin activated miR-15a expression by human laryngeal cancer cells. Suppression of miR-15a expression reversed the anticancer effect of curcumin on cell proliferation of human laryngeal cancer cells and increased Bcl-2 and PI3K/Akt protein expression in AMC-HN-8 cells treated with 40 µM of curcumin. The results of the present study suggest that curcumin inhibits cell proliferation and promotes apoptosis of laryngeal cancer cells through Bcl-2 and PI3K/Akt, and by upregulating miR-15a.

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Section: Discussionmentioning

confidence: 99%

Curcumin inhibits cell proliferation and promotes apoptosis of laryngeal cancer cells through Bcl-2 and PI3K/Akt, and by upregulating miR-15a

Mou

Zhang

et al. 2017

Oncology Letters

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“…Curcumin treatment significantly downregulated expression of miR-186* in A549/DDP multidrug-resistant human lung adenocarcinoma cells and induced apoptosis (48). Treatment of MCF-7 breast cancer cells with curcumin caused downregulation of Bcl-2 and increased expression of miR-15a and miR-16; silencing of miR-15a and miR-16 by specific inhibitors restored Bcl-2 expression, suggesting that reduced Bcl-2 expression in breast cancer cells after curcumin treatment is due to curcumin ability to upregulate the expression of miR15a and miR-16 (49). A dose-dependent decrease in miR-21 promoter activity and expression following curcumin treatment was inferred due to reduced binding of AP-1 to the promoter and induction of the tumor suppressor gene, programmed cell death protein 4 (Pdcd4), which is a miR-21 target and is overexpressed in RKO and HCT116 human colon cancer cells, promoting invasion and metastasis.…”

Section: Curcuminmentioning

confidence: 99%

Plant Phytochemicals as Epigenetic Modulators: Role in Cancer Chemoprevention

Thakur

Deb

Babcook

et al. 2013

AAPS J

137

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Abstract. In recent years, "nutri-epigenetics," which focuses on the influence of dietary agents on epigenetic mechanism(s), has emerged as an exciting novel area in epigenetics research. Targeting of aberrant epigenetic modifications has gained considerable attention in cancer chemoprevention research because, unlike genetic changes, epigenetic alterations are reversible and occur during early carcinogenesis. Aberrant epigenetic mechanisms, such as promoter DNA methylation, histone modifications, and miRNA-mediated post-transcriptional alterations, can silence critical tumor suppressor genes, such as transcription factors, cell cycle regulators, nuclear receptors, signal transducers, and apoptosis-inducing and DNA repair gene products, and ultimately contribute to carcinogenesis. In an effort to identify and develop anticancer agents which cause minimal harm to normal cells while effectively killing cancer cells, a number of naturally occurring phytochemicals in food and medicinal plants have been investigated. This review highlights the potential role of plant-derived phytochemicals in targeting epigenetic alterations that occur during carcinogenesis, by modulating the activity or expression of DNA methyltransferases, histone modifying enzymes, and miRNAs. We present in detail the epigenetic mode of action of various phytochemicals and discuss their potential as safe and clinically useful chemopreventive strategies.

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“…Genistein (soya) MicroRNAs Cancer prevention and therapy Iorio et al (21) Retinoic acid (carrots, spinach, eggs) Histone modifications; microRNAs Cancer prevention and therapy Yang et al (24) Sulforaphane (broccoli) Histone modifications Cancer prevention Ficz et al…”

Section: Effects Of Nutritional Factors On Dna Methylationmentioning

confidence: 99%

Epigenetic mechanisms elicited by nutrition in early life

et al. 2011

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A growing number of studies focusing on the developmental origin of health and disease hypothesis have identified links among early nutrition, epigenetic processes and diseases also in later life. Different epigenetic mechanisms are elicited by dietary factors in early critical developmental ages that are able to affect the susceptibility to several diseases in adulthood. The studies here reviewed suggest that maternal and neonatal diet may have long-lasting effects in the development of non-communicable chronic adulthood diseases, in particular the components of the so-called metabolic syndrome, such as insulin resistance, type 2 diabetes, obesity, dyslipidaemia, hypertension, and CVD. Both maternal under-and over-nutrition may regulate the expression of genes involved in lipid and carbohydrate metabolism. Early postnatal nutrition may also represent a vital determinant of adult health by making an impact on the development and function of gut microbiota. An inadequate gut microbiota composition and function in early life seems to account for the deviant programming of later immunity and overall health status. In this regard probiotics, which have the potential to restore the intestinal microbiota balance, may be effective in preventing the development of chronic immune-mediated diseases. More recently, the epigenetic mechanisms elicited by probiotics through the production of SCFA are hypothesised to be the key to understand how they mediate their numerous health-promoting effects from the gut to the peripheral tissues.

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Curcumin reduces the expression of Bcl-2 by upregulating miR-15a and miR-16 in MCF-7 cells

Cited by 199 publications

References 20 publications

Curcumin inhibits cell proliferation and promotes apoptosis of laryngeal cancer cells through Bcl-2 and PI3K/Akt, and by upregulating miR-15a

Curcumin inhibits cell proliferation and promotes apoptosis of laryngeal cancer cells through Bcl-2 and PI3K/Akt, and by upregulating miR-15a

Plant Phytochemicals as Epigenetic Modulators: Role in Cancer Chemoprevention

Epigenetic mechanisms elicited by nutrition in early life

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