Silencing of CtBP1 suppresses the migration in human glioma cells

Abstract

Carboxyl-terminal binding protein 1 (CtBP1), up-regulated in various types of human cancers, has been functionally associated with proliferation, anti-apoptosis, and EMT in vitro studies. However, the functional significance of CtBP1 in the pathophysiology of glioma remains unknown. In the present study, we showed the expression of CtBP1 was markedly higher in glioma tissues compared with normal brain tissues by Western blot analysis. Immunohistochemical analysis revealed that CtBP1 mainly localized in the nucleus of glioma cells. Statistical analysis suggested the upregulation of CtBP1 was considerably correlated with the WHO grade (P < 0.05) and those patients with high CtBP1 levels exhibited shorter survival time (P < 0.01). Silencing CtBP1 by short hairpin RNAi caused an inhibition of cell migration. Moreover, knockdown of CtBP1 increases E-cadherin expression and decreases vimentin expression. These data uncovered that CtBP1 protein is a valuable marker of glioma pathogenic process and that CtBP1 can serve as a novel prognostic marker for glioma therapy.

<p>C-terminal of E1A binding protein 1 enhances the migration of gastric epithelial cells and has a clinicopathologic significance in human gastric carcinoma</p>

“…GC was reported to rank the second leading cause of cancer-specific mortality worldwide.31 With a poor prognosis, 5-year survival rate of GC is less than 20–25% in the USA, China, and Europe.32 However, early GC represents an excellent (over 90%) opportunity of cure through surgical resection.2 As the increasing detection of early GC, biological therapy options have been technologically advanced both curatively and minimally invasively to maintain a good quality of life 1,3. Recently, dysregulated control of CtBPs expression have been revealed to be a vital originating step in the formation of certainhuman tumors 33–35. CtBPs inhibit multiple proapoptotic and epithelial genes, and overexpression of CtBP in human cancer cells promotes the EMT and cancer cell survival 15,16,36.…”

Dysregulation of Macropinocytosis Processes in Glioblastomas May Be Exploited to Increase Intracellular Anti-Cancer Drug Levels: The Example of Temozolomide

“…CTBP1/BARS and its downstream target PLD1 , whose activation triggers the closure and the final fission of macropinosomes from the plasma membrane [9,61,62], were found downregulated in high-grade tumors at the mRNA level herein. Those results are not consistent with previous data indicating positive correlation of Ctbp protein antigen expression with the histopathologic grade of the glioma [63] and worse survival of the patient [64]. The discrepancies could be related to evaluation at the mRNA versus protein expression level.…”

CTBP1 and metabolic syndrome induce an mRNA and miRNA expression profile critical for breast cancer progression and metastasis

“…We also found that CTBP1 protein increased the migratory capability of TNBC MDA-MB-231 and 4T1 cells. These results support previous studies showing that CTBP1 increases migration of hormone sensitive MCF-7 BrCa cells [ 18 ] and other cell types such as glioma cancer cells [ 20 ].…”