https://www.selleckchem.com/products/senaparib.html Further, LINC00467 high expression was associated with shorter overall survival rate in glioblastoma patients. Further, LINC00467 could bind with miR-339-3p, and IP6K2 was targeted by miR-339-3p. IP6K2 expression was regulated by LINC00467/miR-339-3p in a ceRNA pattern. Moreover, LINC00467 could regulate the development of glioblastoma via miR-339-3p/IP6K2 axis. CONCLUSIONS LINC00467 knockdown repressed cell proliferation but stimulated cell apoptosis in glioblastoma via miR-339-3p/IP6K2 axis, which may enlighten to find a novel therapeutic tactic for glioblastoma patients.BACKGROUND ARHGDIB, a Rho GDP dissociation inhibitor protein, has been reported playing critical roles in regulation of multiple biological responses. However, whether ARHGDIB serves as a valuable biomarker in cancer is little known so far, especially in breast cancer. OBJECTIVE In this study, we aimed to investigate the importance of ARHGDIB in breast cancer, including but not limited to biomarker-like role, as well as potential mechanisms. METHODS Total 100 breast cancer samples and 100 benign breast disease samples were enrolled and underwent detailed pathological assessment and IHC analysis. Human breast cancer cell lines and epithelial cell line were subjected to siRNA-mediated knock-down, RT-qPCR, western blot, MTT staining, cell cycle assay, transwell analysis respectively. RESULTS We observed the expression of ARHGDIB is significantly higher in human breast cancer tissues compared with the benign tissues. ARHGDIB expression was positively correlated with tumor size, lymph node metastasis and TNM stage in breast cancer patients. Moreover, ARHGDIB depletion decreased proliferation, migration and invasion of breast cancer cells. Furthermore, we found ARHGDIB mediated epithelial-mesenchymal transition, and MMP2 is the key downstream effector of ARHGDIB. CONCLUSIONS Hence, our results suggested the significance and predictive role of ARHGDIB i