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Molecular mechanisms underlying anticancer effects of myricetin

期刊

LIFE SCIENCES
卷 142, 期 -, 页码 19-25

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.lfs.2015.10.004

关键词

Myricetin; Cdk1; Akt; Erk1 and Erk2; Mek1; Jak1; Stat3; Ap-1; Apoptosis; Metastasis

资金

  1. Department of Biotechnology, Ministry of Science and Technology, Government of India [BT/BI/25/015/2012]

向作者/读者索取更多资源

Dietary guidelines published in the past two decades have acknowledged the beneficial effects of myricetin, an important and common type of herbal flavonoid, against several human diseases such as inflammation, cardiovascular pathologies, and cancer. An increasing number of studies have shown the beneficial effects of myricetin against different types of cancer by modifying several cancer hallmarks including aberrant cell proliferation, signaling pathways, apoptosis, angiogenesis, and tumor metastasis. Most importantly, myricetin interacts with oncoproteins such as protein Idnase B (PKB) (Akt), Fyn, MEK1, and JAK1-STAT3 (Janus kinase-signal transducer and activator of transcription 3), and it attenuates the neoplastic transformation of cancer cells. In addition, myricetin exerts antimitotic effects by targeting the overexpression of cyclin-dependent kinase 1 (CDK1) in liver cancer. Moreover, it also targets the mitochondria and promotes different kinds of cell death in various cancer cells. In the present paper, a critical review of the available literature is presented to identify the molecular targets underlying the anticancer effects of myricetin. (C) 2015 Elsevier Inc. All rights reserved.

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