SIM2 regulates the expression of MMP-2 and TIMP-2, which drive its role in glioblastoma cells. SIM2s represses BNIP3, a proapoptotic gene, through its hypoxic response element in PC3 cells. Our gene expression profile in PC3 SIM2low cells showed significant change in PTEN, PI3K/AKT and Toll-like receptor signaling pathways which are involved largely in the tumor progression. PTEN negatively controls the PI3K signaling pathway for cell growth and survival by dephosphorylating the 3 position of phosphoinositides. TLR regulates cell proliferation and survival and central signaling molecules mitogenactivated protein kinase and PI3K play key roles. Our data show that inhibition of Sim2 gene in PC3 cells affects expression of several genes encoding proteins that are organized in a network around p38MAPK. These proteins, which include CCL5, MAPKs, ERK and DDR1, have been reported to be involved in tumor development. The chemokine CCL5 has been reported to be expressed by prostate cells and affect their different extents in both setups, or 2) SIM2 may regulate gene expression of other genes either directly or indirectly. Function analysis also revealed that three functions related to cell metabolism had been dysregulated in the PC3 SIM2low cells. This suggested that SIM2 might have metabolic consequences. We have evaluated the production by PC3 cells of 255 metabolites that encompass a large number of human metabolic pathways. Of these, data were obtained for 239 metabolites. Our analysis revealed significant changes in metabolites that constitute key pathways, such as the purine and pyrimidine pathways. Suppression of SIM2 short isoform by antisense oligonucleotides reduced tumor growth in colon cancer cells and induced CAPAN-1 pancreatic cell death through apoptosis. SIM2s was also reported to be an Carfilzomib clinical trial aggressive prostate cancer biomarker since SIM2s protein was associated with increased preoperative serum prostate specific antigen, high histological grade, invasive tumor growth and increased tumor cell proliferation. A recent study showed that SIIM2s may attenuate cell death processes through BNIP3 repression in PC3AR+ cells. However, knockdown of SIM2s in breast cancer MCF-7 cells increased tumorigenesis and thus showed tumor suppressor activity. Most of the previous studies focused on the SIM2s by either intruding or knockdown of SIM2s, we are lacking of the data clarifying the functional role of SIM2 protein including both of its isoforms. Our study reported a combined role of both isoforms of the SIM2 implicated in the prostate cancer cell. Distinguishing the roles of SIM2s and SIM2L may have more profound meaning to understand the functional role of SIM2 in prostate cancer progression, which is our next step to uncover more significance of this gene. ICs activate various cell types following Fcc receptor and complement receptor binding and lead to a diverse range of effector functions. FccRs play important roles in the initiation and regulation of many immunological processes. The importance of an appropriate balance between activating and inhibitory FccRs in the regulation of animal models of arthritis is well recognised. A dominant role for FccRIIIa in IgG IC-mediated inflammatory responses.