It is likely that we saw no effect in ATRA-treated cells due to the fact that POR silencing was not complete. Previous research has shown that POR is an enzyme important for the maintenance of steroid hormones at the level of the whole organism. Its involvement in regulation of global levels of retinoic acid metabolites was documented, while its involvement in regulation of 1,25D levels was postulated. In this study we have shown for the first time that POR gene and POR protein content are regulated in AML cells by ATRA and by 1,25D. We have also observed that POR protein is present not only in the membrane fraction which contains endoplasmic reticulum, but also in the mitochondria, where it could participate in 1,25D catabolism. These observations suggest that POR might be important for maintaining local intracellular levels of ATRA and 1,25D. Since these two compounds are important for VE-821 myeloid cell differentiation, the disturbances in POR activity or expression levels might contribute to the cancer phenotype of myeloid cells. Larger studies using AML patients’ cells and their comparison to normal blood cells, preferably in mice models, are necessary to investigate this hypothesis. Thus, they play important roles in various biological processes, such as embryo development, cell proliferation and differentiation, and carcinogenesis. A great number of studies have demonstrated that miRNAs function as onco- or tumor suppressor genes and that their aberrant expression contributes to human diseases such as cancer. To date, extensive studies have reported aberrant expression of miRNAs such as miR-122, miR-200c, and miR-10b in breast cancer. Further investigation of miRNA involvement in breast cancer could help us better understand the molecular mechanisms responsible for breast cancer development and lead to novel strategies for effective control of breast cancer. The tumor suppressor gene miR-99a is frequently lost or expressed at reduced levels in various human cancers. For example, miR-99a was found to be down regulated in esophageal squamous cell carcinoma tissues and reduced miR-99a expression was correlated with worse overall patient survival. Overexpression of miR-99a by transient gene transfection inhibited esophageal cancer cell proliferation and induced apoptosis. miR-99a was also found to induce cell cycle arrest at G1 phase and suppress tumorigenicity in renal cell carcinoma. Both miR-99a and the related miR-99b can modulate TGF-beta-induced epithelial to mesenchymal transition in normal murine mammary gland cells. Moreover, induction of cell cycle arrest by miR-99a may suppress expression of insulin-like growth factor 1 receptor and mammalian target of rapamycin in hepatocellular carcinoma cells. Expression of miR-99a inhibits the growth of prostate cancer cells and reduces the expression of prostate-specific antigen by targeting chromatin-remodeling factors such as SMARCA5, SMARCD1 and the growth regulator kinase mTOR in vivo.