It noted the effect of curcumin on miRNA expression signatures in pancreatic cancer cells. Curcumin treatment causes downregulation of 18 miRNAs and upregulation of 1-1 miRNAs, including biomedical library, which targets specificity protein 1 and estrogen receptor 1 interpretation. Research of the effect of curcumin on miRNA expression patterns in lung cancer cells reviews the upregulation of four miRNAs and the downregulation of two miRNAs. Apparently, by understanding the effects of curcumin on miRNA term, Zhang et al. Unveiled still another miRNA mediated pro apoptotic mechanism: they noted that curcumin represses the expression of miR 186, which will be involved with the pathogenesis of the multiple drug resistant lung cancer cell line A549/DDP. Curcumin is thought to both prevent lung cancer cell growth and induce apoptosis through the regulation of various specific miRNAs, as an example, curcumin downregulates the potential oncomir miR 186. More over, curcumin induces apoptosis in MCF 7 cells by upregulating the expression of miR 15a and miR 16, ultimately causing the downregulation of the anti apoptotic BCL2 gene, that will be frequently overexpressed in cancer cells. How curcumin influences miRNA phrase remains risky, but, curcumin is famous to bind to DNA methyltransferase 1 and to dam histone acetyltransferases and histone deacetylases, therefore promoting DNA demethylation and histone acetylation and deacetylation, respectively. Subsequently, curcumin likely induces DNA demethylation and histone acetylation, Chromoblastomycosis thus activating the expression of numerous epigenetically silenced miRNAs. While curcumin has a high in vitro activity, its effects are drastically limited by a low bioavailability in vivo. Consequently, new strategies for curcumin supply to and in malignant cells must be established. Appropriately, the usage of a synthetic curcumin analogue represses miR 200 and miR 21 expression, ultimately causing induction of PTEN expression in pancreatic cancer cells. The vitamin A metabolite all trans retinoic acid plays a vital part in HOX gene mediated axis determination all through embryogenesis. The presence of ATRA causes dimerization of retinoic acid receptor and retinoid X receptor. The causing heterodimer therefore binds to DNA in regions called natural product library retinoic acid response elements and transactivates genes involved with development and differentiation. ATRA is presented in combination with chemotherapy to patients experiencing acute promyelocytic leukemia seen as an the promyelocytic retinoic receptor alpha fusion gene, which interferes with cell differentiation and blocks blood cell growth. Profiling of miRNA expression in ATRA treated APL cell lines unveiled whereas miR 181b was downregulated the upregulation of miR 15a, miR 15b, miR 16 1 miR 223, miR 342, miR 107 and many allow 7 family members.