Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glioblastoma multiforme (GBM) is the most common and most malignant type of primary adult brain cancer. The most common phenotype associated with GBM is cellular invasion; however, the molecular mechanisms governing this process are poorly understood. Targeting protein for Xenopus kinesin-like protein 2 (TPX2) is a nuclear protein with roles in cellular proliferation and mitotic spindle assembly. TPX2 is overexpressed in various malignancies, including human malignant astrocytoma. Despite this finding, the exact role of TPX2 in human glioma is not well defined. The present study reports the elevated expression of TPX2 in a number of glioma cell lines. TPX2 overexpression promoted cellular proliferation, decreased the percentage of cells in G0/G1 phase, and increased invasion of both U251 and U87 cells. Overexpression of TPX2 also significantly enhanced the phosphorylation of AKT, decreased the expression of p21, and increased the expression of cyclin D1 and matrix metallopeptidase (MMP)-9. In both U251 and U87 cells, knockdown of TPX2 resulted in phenotypes that are in direct contrast to those observed following TPX2 overexpression. Specifically, TPX2 knockdown inhibited cell proliferation, increased the percentage of cells in G0/G1 phase, inhibited invasion, decreased AKT phosphorylation, decreased the expression of MMP-9 and cyclin D1, and increased p21 expression. The AKT inhibitor IV in large part phenocopied the effect of TPX2 knockdown. The present data suggest that TPX2 promotes glioma cell proliferation and invasion via AKT signaling.
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PMID:TPX2 promotes glioma cell proliferation and invasion via activation of the AKT signaling pathway. 2810 8

MicroRNA-1294 (miR-1294) has been reported to be involved in the progression of esophageal squamous cell carcinoma. However, the function and the mechanisms of miR-1294 in glioma remain unclear. In this study, we explore the potential biological roles of miR-1294 in glioma cell lines. First, we detected the aberrant down-regulation of miR-1294 in glioma tissues and cell lines. Second, we determined that miR-1294 suppresses the proliferation, migration and invasiveness and enhances the chemosensitivity of glioma cells lines to temozolomide. Third, we found that the targeting protein for Xenopus kinesin-like protein 2 (TPX2) is the functional target of miR-1294; miR-1294 acts through TPX2 to exert an important biological effect in glioma. Importantly, TPX2 knockdown had the same effect on glioma cell lines as miR-1294 overexpression. In addition, when TPX2 was up-regulated in these cells, the effects of miR-1294 on glioma cell lines were suppressed. Moreover, the effect of miR-1294 on glioma was verified using a xenograft model. These findings demonstrated that miR-1294 inhibits the development of glioma by targeting TPX2. These findings provide a new potential therapeutic target for glioma treatment.
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PMID:MicroRNA-1294 inhibits the proliferation and enhances the chemosensitivity of glioma to temozolomide via the direct targeting of TPX2. 2951 99