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Figure 2. Mechanisms by which SND1 promotes oncogenesis. Downstream molecules that are upregulated, downregulated or degraded due to over expression of SND1 causing a variety of functions to go into disarray leading to tumorigenesis. Each color represents the specific cancer in which the mechanism has been studied. In prostate cancer regulation of spliceosome assembly by SND1 results in the production of an oncogenic variant of CD44 that promotes proliferation, motility and invasion. Tumor suppressor mRNAs that are targets of oncogenic miRNAs are degraded when SND1 over expression confers increased RISC activity in human HCC cells. SND1 increases AT1R mRNA stability, causing an increase in AT1R levels resulting in activation of ERK and TGFβ signaling pathway, promoting EMT and migration and invasion by human HCC cells. SND1 mediates endonucleolytic decay of tumor suppressor miRNAs in HEK293T cells promoting upregulation of oncogenic proteins. In breast cancer cells, SND1 promotes expression of the E3 ubiquitin ligase Smurf1, leading to RhoA ubiquitination and degradation, disrupting F-actin cytoskeletal organization, increasing cell migration and invasion, and promoting metastasis. SND1: staphylococcal nuclease and tudor domain containing 1; HCC: hepatocellular carcinoma