Past reports suggest that in breast cancer MCF7 cells resveratrol showed aweak DNMT inhibitory activity and was struggling to reverse the methylation of a few tumefaction suppressor genes. Experience of resveratrol increased the activity of adenosine analogues to prevent methylation of the promoter of RARb2 gene which correlated with increase term but resveratrol alone was ineffective. Previous studies demonstrate that resveratrol targets on the type III HDAC, SIRT1, SIRT2, SIRT3 and p300. Triggered Ivacaftor molecular weight SIRT1 adversely adjusts survivin expression through its deacetylase activity. SIRT1 also plays critical role in the aging processes. In breast cancer, human BRCA1 is related to lower quantities of SIRT1 expression. It has been reported that resveratrol can raise the expression of human BRCA1 by transforming H3 acetylation,which is definitely an important technique for specific therapy for BRCA1 associated breast cancer. In vivo studies on APC/ rats show similar results that SIRT1 encoded proteins are required for resveratrol mediated tumor growth inhibition. In prostate cancer, it’s been reported that resveratrol regulates cell survival and/or Chromoblastomycosis apoptosis by worldwide modulation of gene expression through deacetylation of FOXO transcription factor. In vivo study of KrasG12D mice suggested that resveratrol prevents the expression of transcription factor which are required to maintain self and pleuripotency alternative capacity of pancreatic CSC cells. In the case of human SW480 colon cancer cells, reduction in the levels of several oncogenic miRNAs targeting genes encoding Dicer1, a cytoplasmic RNase III making mature miRNAs from their immediate precursors and tumor suppressor facets PDCD4 and PTEN have now been shown after treating with the resveratrol. This research on miRNA mentioned that resveratrol therapy significantly upregulated the expression of 22 miRNA and downregulated 26 miRNA. Several of the downregulated miRNAs include miR 17, miR 21, miR 25, miR 92a 2, constitutively upregulated in cancer of the colon. The level of miR 663 was increased after treatment, which possess putative tumefaction suppressor functions and targets TGF1 transcript. Resveratrol treatment also up-regulated components of the TGFB signaling process, including TGFB receptors type I and type II and down-regulated the transcriptional activity of canonical TGFB key effectors proteins, SMADs. It has been shown that resveratrol in combination with tea polyphenols control the mouse skin cancer development via inhibition of activated MAPKs and p53 pathway. Curcumin, a diferuloylmethane, is just a polyphenol that extracts from the most popular Indian spices turmeric. It is responsible for the yellow pigmentation of curry and is a principal element of the spice turmeric. It’s been associated with numerous health advantages including cancer prevention.