Effects of curcumin on the gene expression profile of L-02 cells

Abstract

Abstract. Curcumin has been utilized in the treatment and prevention of disease, including cancer and cardiovascular disease, but the molecular mechanism behind such numerous effects remains unclear. To explore the molecular mechanism and action sites of curcumin at the cellular level, human hepatic L-02 cells were used to assess these effects. Microarray technology was employed to detect the gene expression of L-02 cells treated with curcumin. According to the microarray results and the data from the National Center for Biotechnology Information, the present study classified and concluded that these curcumin-sensitive genes were associated with diseases and their signaling pathway. The study supports the evidence for treating cancer and cardiovascular disease, and found certain potential marker genes for conducting systematic research into the effects of curcumin. A total of 80 genes were identified as significantly differentially expressed between samples treated with and without curcumin. Curcumin is capable of developing physiological reactions and functions by regulating the gene expression and affecting its signal transduction pathway. Tumor protein p63, MYC-associated factor X and certain other genes associated with tumors act on a potential therapeutic target, while apolipoprotein B receptor and oxysterol-binding protein-like 7, and their signaling pathways may be involved in the cardioprotective effects of curcumin.

RNA-Seq Analysis Reveals Candidate Targets for Curcumin againstTetranychus cinnabarinus

“…As a botanical compound extracted from Curcuma longa , curcumin has various pharmacological activities, especially strong anticancer activity. Curcumin can affect and disrupt the proliferation, growth, and metabolism of tumor cells, as well as promote apoptosis [ 32 , 33 ]. The inhibition of ornithine decarboxylase, c- myc , Akt, and protein kinase C is considered the major molecular mechanism of curcumin as a pharmaceutical [ 34 – 38 ].…”

PDGF signaling pathway in hepatic fibrosis pathogenesis and therapeutics

“…Curcumin, the principal component of the spice turmeric and certain herbal medicines ( Zedoariae rhizome and Radix Curcumae ), is able to inhibit epithelial-to-mesenchymal transition and affect numerous intracellular targets, involving certain miRNAs, and the estrogen receptor, nuclear factor-like 2, insulin-like growth factor-1 and PI3K/Akt signaling pathways ( 100 – 103 ). Due to its numerous potential effects, including anti-inflammatory, hypolipidemic, hypoglycemic and chemopreventive activity, curcumin may increase antioxidant enzyme activities, activate cytochrome P4502E1 and concomitantly suppress the activity of fatty acid synthase, β-catenin transactivation and DNA-binding ( 104 , 105 ).…”

Verapamil Inhibits TRESK (K2P18.1) Current in Trigeminal Ganglion Neurons Independently of the Blockade of Ca2+ Influx

“…These results indicate that verapamil inhibits TRESK current independently of the blockade of Ca 2+ influx. Similar to TRESK channels, Kv channels expressed in smooth muscle cells isolated from a rabbit coronary artery are inhibited by verapamil independently of any Ca 2+ channel inhibition [ 23 ]. Verapamil is known to block many types of K + channels, such as ATP-sensitive K + channel [ 24 ], inactivating delayed K + channel [ 25 ], Kv1.1, Kv1.5, Iks, hERG [ 26 ], and Kv1.3 [ 27 ].…”