Hassan Faiz-Ul, Rehman Muhammad Saif-Ur, Khan Muhammad Sajjad, Ali Muhammad Amjad, Javed Aroosa, Nawaz Ayesha, Yang Chengjian
Key Laboratory of Buffalo Genetics, Breeding and Reproduction Technology, Ministry of Agriculture and Guangxi Buffalo Research Institute, Chinese Academy of Agricultural Sciences, Nanning, China.
Institute of Animal and Dairy Sciences, University of Agriculture Faisalabad, Faisalabad, Pakistan.
Front Genet. 2019 Jun 4;10:514. doi: 10.3389/fgene.2019.00514. eCollection 2019.
Curcumin (a polyphenolic compound in turmeric) is famous for its potent anti-inflammatory, anti-oxidant, and anti-cancer properties, and has a great potential to act as an epigenetic modulator. The epigenetic regulatory roles of curcumin include the inhibition of DNA methyltransferases (DNMTs), regulation of histone modifications via the regulation of histone acetyltransferases (HATs) and histone deacetylases (HDACs), regulation of microRNAs (miRNA), action as a DNA binding agent and interaction with transcription factors. These mechanisms are interconnected and play a vital role in tumor progression. The recent research has demonstrated the role of epigenetic inactivation of pivotal genes that regulate human pathologies such as cancers. Epigenetics helps to understand the mechanism of chemoprevention of cancer through different therapeutic agents. In this regard, dietary phytochemicals, such as curcumin, have emerged as a potential source to reverse epigenetic modifications and efficiently regulate the expression of genes and molecular targets that are involved in the promotion of tumorigenesis. The curcumin may also act as an epigenetic regulator in neurological disorders, inflammation, and diabetes. Moreover, curcumin can induce the modifications of histones (acetylation/deacetylation), which are among the most important epigenetic changes responsible for altered expression of genes leading to modulating the risks of cancers. Curcumin is an effective medicinal agent, as it regulates several important molecular signaling pathways that modulate survival, govern anti-oxidative properties like nuclear factor E2-related factor 2 (Nrf2) and inflammation pathways, e.g., nuclear factor kappa B (NF-κB). Curcumin is a potent proteasome inhibitor that increases p-53 level and induces apoptosis through caspase activation. Moreover, the disruption of 26S proteasome activity induced by curcumin through inhibiting DYRK2 in different cancerous cells resulting in the inhibition of cell proliferation opens up a new horizon for using curcumin as a potential preventive and treatment approach in proteasome-linked cancers. This review presents a brief summary of knowledge about the mechanism of epigenetic changes induced by curcumin and the potential effects of curcumin such as anti-oxidant activity, enhancement of wound healing, modulation of angiogenesis and its interaction with inflammatory cytokines. The development of curcumin as a clinical molecule for successful chemo-prevention and alternate therapeutic approach needs further mechanistic insights.
姜黄素(姜黄中的一种多酚化合物)以其强大的抗炎、抗氧化和抗癌特性而闻名,并且具有作为表观遗传调节剂的巨大潜力。姜黄素的表观遗传调控作用包括抑制DNA甲基转移酶(DNMTs)、通过调节组蛋白乙酰转移酶(HATs)和组蛋白去乙酰化酶(HDACs)来调节组蛋白修饰、调节微小RNA(miRNA)、作为DNA结合剂以及与转录因子相互作用。这些机制相互关联,在肿瘤进展中起着至关重要的作用。最近的研究已经证明了关键基因的表观遗传失活在调节人类疾病如癌症中的作用。表观遗传学有助于理解通过不同治疗药物进行癌症化学预防的机制。在这方面,膳食植物化学物质,如姜黄素,已成为逆转表观遗传修饰并有效调节参与肿瘤发生促进过程的基因和分子靶点表达的潜在来源。姜黄素在神经疾病、炎症和糖尿病中也可能作为表观遗传调节剂发挥作用。此外,姜黄素可以诱导组蛋白修饰(乙酰化/去乙酰化),这是导致基因表达改变从而调节癌症风险的最重要的表观遗传变化之一。姜黄素是一种有效的药物,因为它调节多种重要的分子信号通路,这些通路调节细胞存活、控制抗氧化特性如核因子E2相关因子2(Nrf2)以及炎症通路,例如核因子κB(NF-κB)。姜黄素是一种有效的蛋白酶体抑制剂,可提高p-53水平并通过半胱天冬酶激活诱导细胞凋亡。此外,姜黄素通过抑制不同癌细胞中的DYRK2诱导26S蛋白酶体活性的破坏,从而导致细胞增殖的抑制,这为将姜黄素用作蛋白酶体相关癌症的潜在预防和治疗方法开辟了新的前景。本综述简要总结了关于姜黄素诱导的表观遗传变化机制以及姜黄素的潜在作用,如抗氧化活性、促进伤口愈合、调节血管生成及其与炎性细胞因子相互作用的相关知识。将姜黄素开发成为成功的化学预防临床分子和替代治疗方法需要进一步的机制见解。