The out put genes in the large network might indeed show caspase-independent cell death mechanism induced by genetically unstable tetrapolidy. The sperm associated antigen 5 was found to be associated with various types of cancer, such as cervical cancer and breast cancer. Circadian regulation of these genes and as such of the processes they regulate could be achieved via a fine-tuning of ROR/REV-ERB. Two other circadian regulated genes identified by our study are nucleolin and Ddx6. The analysis of ChIP-seq data identified these genes as targets of ROR�� and REV-ERB respectively. Interestingly, they were also reported to be involved in miRNA regulation. DDX6 is found in p-bodies for mRNA degradation, needed for miRNA mediated silencing. NCL Palbociclib Isethionate regulates several miRNAs including miR-21, miR-221, miR222and miR-103. miR-21 is PP1 defined as an oncogene and found to be overexpressed in most tumour types, where as miR-221 and miR222 show an increased expression in human breast cancer. Also, miR-222 was shown to promote resistance of cancer cells to cytotoxic Tlymphocytes. Interestingly, miR-103 which is also a target of NCL was reported to exhibit circadian pattern. Altogether, our data allowed the generation of a large network of circadian regulation. The network was retrieved from human expression data intersected with text-mining of the biomedical literature, for topology refinement and denovo target identification. The novel predicted targets of the circadian clock network showed are markable association to cancer driving mechanisms. One of these mechanisms is miRNA regulation. Very recent studies point to an influence of miRNAs on the circadian clock, but only a few links on the regulation of miRNAs via the circadian clock have been described. NCL represents a potential novel link via which the circadian clock, in particular ROR��, regulates the expression of miRNAs, with particular consequences in cancer progression. Upon T cell receptor-mediated recognition of MHC antigenic peptides, T cell responses to antigens, including autoreactive antigens, are or chestrated by a group of cell surface signaling molecules.