Here we investigated whether the cellular accumulation of p53 protein caused by over-expression of small ubiquitin-related modifier-1 (SUMO-1) could be used as a predictive marker for prognosis in colon cancer. We detected SUMO-1 and p53 protein levels in 46 cases of colon cancer and adjacent tissues by immunohistochemistry and found that SUMO-1 was expressed at much higher levels in colon cancer compared with that in normal colon tissue. Immunoprecipitation and Western blot analysis revealed that the tumor suppressor p53 was present predominantly in the sumoylated rather than the non-sumoylated form in the colon cancer cell lines. A small interfering RNA targeted to SUMO-1 mRNA sequences was used to observe the levels of the p53 protein. Patients who showed high dual expressions of SUMO-1 and p53 tended to experience metastasis more frequently. These results suggest that the cellular accumulation of p53 protein caused by over-expression of SUMO-1 may be involved in tumor aggressiveness. Multivariate analysis confirmed that the high dual expression of SUMO-1 and p53 was an independent factor for evaluating prognosis. SUMO-1 may be useful as a novel target for therapy in colon cancer as well as a clinical indicator for tumor aggressiveness.

Background Long non-coding RNAs (lncRNAs) have been discovered to participate in various cancer developments. However, the biological function of lncRNAs associated with gastric cancer (GC) has not been fully elucidated. Methods Quantitative RT-PCR (qRT-PCR) assay was performed to measure lncRNAs, microRNAs (miRNAs) and message RNA (mRNA) expression. Cell Counter Kit-8 (CCK-8), clone formation, wound healing, and transwell assays were performed to investigate cell proliferation, migration, invasion, and apoptosis. Fluorescence in situ hybridization (FISH) assay was used to analyze LINC00922 in either the cytoplasm or nucleus. The potential binding among lncRNA, miRNA, and mRNA was evidenced by bioinformatics, luciferase reporter assay. Mouse-xenograft experiments were used to explore the tumorigenesis in vivo. Results LINC00922 was upregulated in GC, and high LINC00922 expression was associated with poor prognosis. Inhibition of LINC00922 suppressed GC cell proliferation, migration, invasion, and activated cell apoptosis in vitro and inhibited tumorigenesis in vivo. Besides, LINC00922 was markedly located in the cytoplasm. The mechanistic analysis demonstrated that LINC00922 acted as a sponge of miR-204-5p, thereby inhibiting the expression of the target gene-High Mobility Group AT-hook 2 (HMGA2). Conclusion LINC00922 accelerated the progression of GC by miR-204-5p/HMGA2 axis. These findings support LINC00922 may be a promising option for the diagnosis and therapy of GC.