**2.6 (**−**)-Epigallocatechin-3-gallate**

(−)-Epigallocatechin-3-Gallate or EGCG is a major polyphenol compound in green tea (*Camellia sinensis*) and derivative of catechin [3, 16]. EGCG is a powerful antioxidant, anticancer and antiangiogenic properties, which has a potential role to influence human diseases [54–56]. EGCG suppressed nasopharyngeal carcinoma cell migration and invasion through a novel signaling axis of miR-296/STAT3 regulation [57]. Gold nanoparticles (AuNPs) have been used for drug delivery as their stability and increase drug bioavailability as well as accumulation of drug in cancer cells. EGCG-capped gold nanoparticles upregulated the tumor suppressor miRNAs, let-7a and miR34a, which consecutively their targeted gene, caspase-3 was upregulated, and c-Myc protein was decreased in hepatocellular carcinoma cells [58]. miR-34a is one of the tumor suppressor miRNAs that downregulated, whereas miR-93 is highly up-regulated in prostate cancer cells. Co-transfection of miR.34a mimic and miR.93 inhibitor along with EGCG significantly decreased androgen receptor (AR) and prostate-specific antigen (PSA) expression when compared to the co-transfection without EGCG [59]. In cervical carcinoma cells, Hela (HPV16/18+), EGCG inhibited cell growth and up-regulated miR-29 and miR-210 expression, while down-regulated the expression of miR-125b and miR-203 [60]. Up-regulation of let-7 was observed in EGCG treated melanoma cells, which led to inhibit the expression of high mobility group A2 (HMGA2) [61].

EGCG showed the protective effect against myocardial ischemia/reperfusion (I/R) injury through up-regulation of miR-384-mediated autophagy by targeting Beclin-1 via activating the PI3K/Akt signaling pathway [62]. EGCG also demonstrated the anti-arthritic effects by inhibited IL-1β-induced ADAMTS5 expression and up-regulated the expression of miR-140-3p in osteoarthritis chondrocytes [63]. EGCG treatment has potential role of preventing toxin-induced fibrosis by suppression of osteopontin expression and up-regulation of miR-10b, miR-181a and miR-221 in liver hepatocellular carcinoma cells [64].

#### **2.7 Genistein**

Genistein belongs to isoflavone family and presents in soybeans with antiangiogenic, anti-metastasis, anti-inflammatory, anti-oxidant, cell cycle arrest and induction of apoptosis effects [65]. Genistein can regulate the expression of miRNAs in several call types [65]. It has been reported that treatment of genistein up-regulated miR-23b and inhibited breast cancer cell growth [66]. Genistein also exhibited anti-tumor effect

#### *The Impact of Dietary Compounds in Functional Foods on MicroRNAs Expression DOI: http://dx.doi.org/10.5772/intechopen.96746*

by down-regulated miR-1260b and targeting sRRP1 and Smad4 through DNA methylation or histone modifications in prostate cancer cells [67]. The same research group reported that miR-1260b was highly expressed in renal cancer cells and miR-1260b was down-regulated in genistein treated renal cancer cells [68]. The treatment of miR-1260b inhibitor inhibited the expression of its target genes, sFRP1, Dkk2, Smad4 [68]. Treatment with genistein induced non-small lung cancer cell apoptosis, caspase-3/9 activation and inhibited cell proliferation via up-regulation of miR-27a -mediated MET signaling [69]. Co-encapsulate miR-29b with genistein in hybrid nanoparticles (GMLHN) has been studied to treat effectively in non-small lung cancer cell and GMLHN showed the anti-proliferative effect by down-regulation of phosphorylated AKT (pAKT) and phosphorylated phosphoinositide-3 kinase (p-PI3K) [70].

Genistein promoted myoblast proliferation and differentiation through downregulated miR-222 expression, resulting in increased expression of its target genes, MyoG, MyoD, and ERα [71]. Interestingly, genistein up-regulated miR-451 expression and inhibited IL1β expression and inflammation in chronic liver disease nonalcoholic steatohepatitis (NASH) mice model [72].
